Carbofuran-Induced Alterations in Body Morphometrics and Histopathology of Liver and Kidneys in the Swiss Albino Mice Mus Musculus L

8/11/2019 Carbofuran-Induced Alterations in Body Morphometrics and Histopathology of Liver and Kidneys in the Swiss Albin

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International Journal of Scientific Research in Environmental Sciences, 2(9), pp. 308-322, 2014Available online at http://www.ijsrpub.com/ijsres

ISSN: 2322-4983; 2014 IJSRPUBhttp://dx.doi.org/10.12983/ijsres-2014-p0308-0322

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Full Length Research Paper

Carbofuran-Induced Alterations in Body Morphometrics and Histopathology ofLiver and Kidneys in the Swiss Albino Mice M us M usculu s L.

M. Saiful Islam 1*, Moni Krishno Mohanta 1, Ananda Kumar Saha 1, Anup Mondol 1, M. Mizanul Hoque 1, ApurbaKumar Roy 2

1Genetics and Molecular Biology Laboratory, Department of Zoology, University of Rajshahi, Rajshahi 6205, Bangladesh2Department of Genetic Engineering and Biotechnology, University of Rajshahi, Rajshahi 6205, Bangladesh

*Corresponding author; email: [email protected]

Received 03 June 2014; Accepted 08 August 2014

Abstract. Carbofuran-fed changes in body, liver and kidney weights as well as alterations in the histopathology of hepatic andrenal tissues in the Swiss albino mice Mus musculaus L. were assessed. Twenty 7-10 days old male mice were divided equallyinto five groups viz . T0 (control), T1, T2, T3 and T4, which were allowed to feed on Carbofuran supplemented diets at doses of0.0 (control), 0.5, 1.0, 1.5 and 2.0 mg/kg food. Compared to the decrease in body and kidney weights of the treated mice,Carbofuran-fed diets resulted in a significant gain in both body (P


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Mice M us M usculus L .

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bendary et al., 2014). This led to design the presentinvestigation.

Carbofuran-induced damages in a number oforgans and/or systems in rodents have previously beenreported. Thus reproductive organs (Aziz et al., 2008)and thyroid glands (Hadie et al., 2012) in male rats,tissues of tail muscles and liver in toad tadpoles(Jayatillake et al. (2011) and testes (Al-Amoudi,2012) and testosterone serum concentration in mice(Elayan et al. (2013) showed remarkable Carbofurantoxicity.

Apart from the aforesaid carbamate injury and poisoning in mice and rats, however, a number ofother insecticides and cytotoxic chemicals, forexamples, organochlorine such as Endosulfan(Aleksandrowiez, 1997; Choudhury et al., 2003),

organophosphate like Chlorpyriphos and Profenofos(Saha et al., 2006; Dessouki et al., 2013; El-bendary etal., 2014), pyrethroid like Cypermethrin(Khalequzzaman et al., 2004; Yavasoglu et al., 2006),and cisplatin (Adejuwon et al., 2014) have also beentested to assess their histopathological impacts on theexperimental rodents. Taking these findings inconsideration, the present investigation was designedto observe a detailed account of Carbofuran-inducedchanges in body, liver and kidney weights andhepatosomatic and renosomatic indices, along withhistopathological alterations in the tissues of liver and

kidneys in the male Swiss albino mice underlaboratory conditions.

2. MATERIALS AND METHODS

2.1. Test animals

Seven to ten days old male Swiss albino mice Musmusculus L. (Rodentia: Muridae) were collected fromthe Animal Resources Branch (ARB), InternationalCentre for Diarrhoeal Disease Research, Bangladesh(ICDDR, B). They weighed between 16 and 24g(mean SD = 21.26 2.34g) and were reared ingroups of four in steel cages of 47cm 37cm 23cmsize with saw dust bedding at 25 2 C and 705%relative humidity (RH) with 14 hr: 10 hr light: dark(L:D) regime and were allowed to acclimatize for a

period of 6-7 days prior to experimental use. The bedding was replaced once a week. The mice weremaintained on a standard diet composed of maizegrain (36.92%), rice polish (18.46%), wheat polish(24.62%), soybean (18.46%), crude protein (1.23%),and salt and large grain premix (0.15% each), suppliedtwice daily and all the mice had access to drinkingwater ad libitum . In compliance with the standardanimal ethical guidelines, the present investigationwas carried out at the Laboratory of Genetics andMolecular Biology, Department of Zoology,

University of Rajshahi, Bangladesh, during the periodfrom February 2013 to June 2013.

2.2. Test chemical

Technical grade (99.99%) Carbofuran (product nameAlphafuran 5G) was procured from the Alpha AgroLimited, Dhaka, Bangladesh.

2.3. Experimental design

Twenty male mice were randomly segregated into fivegroups (T0-T4), each having four animals. T0 groupserved as the control which received diets withoutCarbofuran, whereas groups T1-T4 were given atdoses of 0.5 mg/kg, 1.0 mg/kg, 1.5 mg/kg and 2.0

mg/kg Carbofuran supplemented diet, respectively.All the experiments were performed in accordancewith the guidelines for use and care of laboratoryanimals.

2.4. Body, liver and kidney weights

Initial and final body, liver and kidney weights of thecontrol and treatment groups of mice were recordedduring the experiment. After 15, 25, 35 and 45 days

post-treatment just before sacrificing the animals, themorphometric measurements were recoded again. The

mice to be sacrificed were placed in a jar containingcotton wool soaked in diethyl ether. Completeanaesthesia was considered accomplished when the

pedal movements and eye lid reflex disappeared andthe animal became recumbent while still breathing.The belly of the mice was cut open to collect liver andkidneys which were weighed, gently rinsed in normalsaline, fixed in 10% formalin and stored at 4 C forhistopathology. Finally, hepato- and renosomaticindices were estimated as follows: liver or kidneyweight body weight 100 (El-Damaty et al., 2012;Adejuwon et al., 2014).

2.5. Histopathology

The tissue samples of liver and kidney were quicklyexcised following the protocol of Sarker et al. (2005).Slices of the organs were quickly prepared forhistological examination to show if there weremorphological changes in the organs during thetreatment. Processing started with the parking of thetissues in the tissue capsule. The tissues weredehydrated in graded levels of ethanol (70-100%) inascending order. The alcohol was changed aftersoaking the tissues in them for 1 and 2h. The tissuewere cleared in chloroform and impregnated with

paraffin wax and sectioned at 4-5 thickness using arotary microtome machine. The sections were floated


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on a water bath maintained at 2-3 o C below melting point of paraffin wax. They were on a hot platethermostatically maintained at temperature of 2-3 o Cabove the mid point of paraffin wax when properlydried (15-30 min), they were stained withhaematoxylin and eosin, dehydrated, cleared andmounted in DPX, avoiding air bubbles. Finally,examinations of the slides were made by a lightmicroscope (Zeiss, Germany) and microphotographswere taken with an automated digital camera system(Olympus CH30/CH40, Japan) at suitable but varyingmagnifications of 4 to 40.

2.6. Statistical analyses

Morphometric data on body, liver and kidney weights

were analyzed using SPSS for Windows (version19.0) and presented in mean standard deviation.Experimental data between the control and treatmentgroups were subjected to one-way analysis of variance(ANOVA) followed by the post hoc LSD (leastsignificant difference) tests to separate the means,where the levels of significance were set at P


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Table 1: Effect of Carbofuran treated diet on the relative body, liver and kidney weights (g) of the male Swiss albino mice

Parameters/Treatments

Initial (0 day) 15 days 25 days 35 days 45 days F-values(Probabilities)

Body weight 2.668(0.004)

T0 21.681.50a

22.931.55a

24.171.65a

25.501.84a

28.10T1 21.332.37 a 19.882.73 c 18.402.84 b 15.700.28

c 15.00

T2 21.203.08 a 19.552.80 c 19.171.96 b 16.351.63c 15.20

T3 20.503.12 a 20.233.14 b 20.032.28 b 18.402.26 18.10

T4 21.582.55 a 19.202.64 c 17.972.15 b 16.201.70c 15.20

Liver weight(Hepatosomatic index)

3.759 (0.001)(1.750; ns)

T0 1.580.17a

(7.300.94)1.850.21 a (8.08084)

1.670.21 a (6.951.29)

1.600.01 a (6.290.45)

1.60(5.69)

T1 1.400.22 b

(6.550.37)1.350.31 b (6.841.69)

1.070.15 c (5.840.85)

1.200.01 b (7.650.13)

1.20(8.00)

T2 1.380.22(6.581.38)1.380.37(7.031.62)

1.230.15(6.491.09)

1.200.00(7.380.73)

1.00(6.58)

T3 1.330.22(6.470.47) 1.130.19c

(5.590.64) 1.330.06(6.700.71) 1.150.07(6.280.39) 1.10(6.08)

T4 1.330.19(6.160.39)1.100.22 c (5.710.69)

1.00020 c (5.530.46)

0.950.21 c (5.830.70)

0.80(5.26)

Kidney weight(Renosomatic index)

2.045 (0.025)(2.822; 0.002)

T0 0.550.03a

(2.520.08)0.550.05 a (2.390.05)

0.570.02 a (2.350.07)

0.550.04 a (2.160.01)

0.62(2.21)

T1 0.480.02 b

(2.260.24)0.520.03 a (2.610.18)

0.500.03 b (2.760.24)

0.470.01 b (3.000.04)

0.46(3.07)

T2 0.530.03a

(2.530.44)0.510.03 a (2.610.24)

0.530.01(2.800.24)

0.490.01(3.010.21)

0.48(3.16)

T3 0.560.02a

(2.760.43)0.540.02 a (2.710.34)

0.520.05(2.600.05)

0.500.06(2.720.03)

0.54(2.98)

T40.540.03 a (2.500.26)

0.510.03 a (2.650.19)

0.530.04 b (2.940.13)

0.490.04 b (3.030.06)

0.48(3.16)

Values are mean SD; dissimilar superscript letters for a parameter or treatment in the same column differ significantly by (LSD) tests (P


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Plate 1: Transverse sections of liver of Carbofuran treated mice after 15 days. Slides for the control (T0) and treatment groups(T1-T4) are designated by 1.C, 1.1, 1.2, 1.3 and 1.4, respectively. Abbreviations: BD= bile duct; BH= bi-nucleated

hepatocytes; CV= congested vein; DS= dilated sinusoid; FCV= fibre-deposited central vein; FPV= fibre-deposited portal vein;H= hepatocytes; HA= hepatic artery; HE= haemorrhage; HmE= haemosiderin epithelial cells; HmH= haemosiderin

hepatocytes; HmK= haemosiderin Kupffer cells; K= Kupffer cells; PV= portal vein; SPV= shrunken portal vein.


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Plate 2: Transverse sections of liver of Carbofuran treated mice after 25 days. Slides for the treatment groups (T1-T4) aredesignated by 2.1, 2.2, 2.3 and 2.4, respectively. Abbreviations: BH= bi-nucleated hepatocytes; CA= congested area; CBD=

congested bile duct; CCV= congested central vein; CDB= cell debris; CPV= congested portal vein; CV=; congested vein;DCV= dilated central vein; DS= dilated sinusoid; HE= haemorrhage; HmH= haemosiderin hepatocytes; HmK= haemosiderin

Kupffer cells; PV= portal vein.

Plate 3: Transverse sections of liver of Carbofuran treated mice after 35 days. Slides for the treatment groups (T1-T4) aredesignated by 3.1, 3.2, 3.3 and 3.4, respectively. Abbreviations: BD= bile duct; BH= bi-nucleated hepatocytes; CBD=congested bile duct; CCV= congested central vein; CPV= congested portal vein; CV= central vein; DS= dilated sinusoid; F=

fibrous tissue; FCV= fibre-deposited central vein; HE= haemorrhage; HmE= haemosiderin epithelial cells; HmK=haemosiderin Kupffer cells; INF= inflammatory cell infiltration; NH= necrotic hepatocytes; PV= portal vein; V= vacuolation.


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Plate 4: Transverse sections of liver of Carbofuran treated mice after 45 days. Slides for the treatment groups (T1-T4) aredesignated by 4.1, 4.2, 4.3 and 4.4, respectively. Abbreviations: BD= buile duct; CBD= congested bile duct; CDB= cell

debris; CV= central vein; DPV= dilated portal vein; DS= dilated sinusoid; EC= enucleated cells; FPV= fibre-deposited portalvein; HE= haemorrhage; HmH= haemosiderin hepatocytes; HmK= haemosiderin Kupffer cells; IMC= increased number of

mononuclear cells; INF= inflmmatory cell infiltration.

Table 2: Major histopathological changes detected before and after Carbofuran treatments in the Swiss albino miceTreatment groups/

OrgansMajor histopathological changes Severity 1

LiverT0 Usual structures of the hepatocytes with normal central vein, Kupffer cells and sinusoids _

T1 Shrunken portal vein and haemosiderin in Kupffer cells; binucleated hepatocytes, haemosiderin inhepatocytes, fibrous central and portal veins; haemosiderin in epithelial cells; haemorrhage anddilated sinusoids

+

T2 Haemorrhage accompanied by cell debris, vacuolated and congested central vein; haemorrhage anddilated sinusoid; congested portal vein, cell debris and vacuolation; and congested area and dilatedcentral vein

++

T3 Necrotic hepatocytes and congested portal vein; fibre deposited central vein; inflammatory cellinfiltration and congested central vein; and fibrous tissue accompanied by inflammatory cellinfiltration

+++

T4 Haemorrhage and inflammatory cell infiltration; increased number of mononuclear cells and dilated portal vein; fibre-deposited portal vein accompanied by cell debris and haemorrhages; andenucleated cells, necrotic hepatocytes and increased number of mononuclear cells

++++

KidneyT0 Normal arrangements of Bowmans capsule, glomerulus, urinary pulp, distal and proximal

convoluted tubules and podocytes _

T1 Oedema and congested glomerulus accompanied by widened urinary space; inflammatory cellinfiltration and vacuolated tubules; dilated collecting duct, medullary ray and distal tubule, increasednumber of mesangial cells and degenerated glomerulus

+

T2 Dilated collecting ducts, vacuolated tubules, cell debris, congested glomerulus and widened urinaryspace; shrunken glomeruli, presence of inflammatory cell infiltration and hyalinized area; dilatedtubule, eroded wall of Bowmans capsule and increased number of podocytes

++

T3 Haemorrhage accompanied by degenerated or congested glomerulus and widened urinary space;dilated proximal tubule and increased number of mesangial cells; inflammatory cell infiltration anddilated tubule; and vacuolated tubule and degenerated Bowmans capsule

+++

T4 Vacuolated distal tubule and haemorrhage; dilated collecting and proximal tubules and degeneratedglomerulus; increased number of podocytes, large mononuclear cells and eroded wall of Bowmanscapsule; and shrinkage of proximal tubule, increased number of podocytes and haemorrhage

++++

1 _ = no change; += minor; ++=not severe; +++= severe; ++++=very severe.


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3.3. Histopathology of kidney

The transverse sections of untreated control renal cellsrevealed normal arrangements of Bowmans capsule,glomerulus, urinary pulp, distal and proximalconvoluted tubules and podocytes (Plate 5.C). Incontrast, the Carbofuran-treated feed induced thefollowing exposure-dependent symptoms in theexperimental mice (summarized in Table 2):

15 days post-treatment: At lower doses oedemaand congested glomerulus (Plate 5.1); congestedglomerulus accompanied by widened urinary space(Plate 5.2); while a higher doses inflammatory cellinfiltration and vacuolated tubules (Plate 5.3); anddilated collecting duct, medullary ray and distaltubule, increased number of mesangial cells and

degenerated glomerulus (Plate 5.4) were commonfeatures.25 days post-treatment: Such symptoms as dilated

collecting ducts, vacuolated tubules, cell debris,congested glomerulus and widened urinary space(Plate 6.1); shrinkage of glomerulus, inflammatorycell infiltration and hyalinized area (Plate 6.2); dilatedtubule, eroded wall of Bowmans capsule andincreased number of podocytes (Plate 6.4) weremanifested.

35 days post-treatment: Haemorrhageaccompanied by degenerated or congested glomerulus

and widened urinary space (Plate 7.1); dilated proximal tubule and increased number of mesangialcells (Plate 7.2); inflammatory cell infiltration anddilated tubule (Plate 7.3); and vacuolated tubule anddegene rated Bowmans capsule (Plate 7.4) weresalient features.

45 days post-treatment: In addition to some of theaforesaid anomalies, vacuolated distal tubule andhaemorrhage (Plate 8.1); dilated collecting and

proximal tubules and degenerated glomerulus (Plate8.2); increased number of podocytes, largemononuclear cells and eroded wall of Bowmanscapsule (Plate 8.3); and shrinkage of proximal tubule,increased number of podocytes and haemorrhage(Plate 8.4) were notable characteristics.

4. DISCUSSION

In this investigation, a detailed account of Carbofuran-fed changes in body, liver and kidney weights,coupled with corresponding toxic effects of thecarbamate insecticide in the liver and kidney tissues ofmale Swiss albino mice has been presented. Theresults of the current study revealed that there weresignificant decreases in body and liver weights in

mice treated with Carbofuran. In toxicological studies,however, organ and relative organ weights areimportant criteria for evaluation of organ toxicity(Crissman et al., 2004). The organ and relative organweights may be increased or decreased depending onthe nature and mode of action of the insecticide.However, the present data corroborate to Pant et al.(1995) and El-Damaty et al. (2012) but differ fromBrkic et al. (2008) where a statistically significantincrease in body weight of male rats treated withCarbofuran at 400 mg/kg body weight was observed.

In an earlier study, Khogali et al. (2005) reportedDimethoate-induced hepatic pycnosis, vacuolation,

blood congestion and high lymphatic infiltrationaround the central vein; and changes in the cortex atthe glomeruli as swollen cellular lining of the

Bowmans capsule in Swiss albino mice. While oraladministration of Carbosulfan at 48 mg/kg/day for 5,10, 20 and 30 days in albino mice resulted in dilationof central vein and sinusoids between hypertrophiedhepatocytes, vacuolization and hyalinization ofhepatocytes with loss of radial arrangement,suggesting that the insecticide had adverse effects onliver functions leading to histological and

physiological impairments (Ksheerasagar andKaliwal, 2006). Further Ksheerasagar and Kaliwal(2010) administered Carbosulfan at 12, 24 mg/kg/dayorally for 30 days in mice and noticed in the loss of

normal arrangement of cortical tubules and formationof vacuoles in hepatic tissues; while Carbosulfan at 36and 48 mg/kg/day for 30 days resulted in atrophiedglomeruli which were loosely attached to Bowmanscapsules. Owing to a prolonged exposure of 45 days,however, the present results appeared to be moredrastic on mice organs than those discussed above.

In Asian common toad tadpoles, Duttaphrynusmelanostictus exposure of 50-500 g/L Carbofuranfor 15 days resulted in greater vacuolation inhepatocytes, sinusoidal dilations and the formation of

bile plugs (Jayatillake et al., 2011). El-Damaty et al.(2012) examined the effects of Carbofuran on liverand kidney function parameters in male albino rats, inwhich 1/10 th of the LD 50 dose resulted in the decreaseof body weight but increased the liver and kidneyweights. Liver histopathology at this dose included

pyknotic nuclei, focal necrosis with inflammatoryinfiltration, vacuolization and blood congestion;whereas kidney histopathology included bloodcongestion in between tubules and small area ofhaemorrhage in the interstitial tissues. These findingsare slightly different from those of the presentobservations perhaps because of different dose levelsand exposure durations.


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Plate 5: Transverse sections of kidney of Carbofuran treated mice after 15 days. Slides for the control (T0) and treatmentgroups (T1-T4) are designated by 5.C, 5.1, 5.2, 5.3 and 5.4, respectively. Abbreviations: BC= Bowmans capsule; CG=

congested glomeruli; DCD= dilated collecting duct; DDT= dilated distal tubule; DG= degenerated glomeruli; DMR= dilatedmedullary ray; DT= dilated tubule; EWB= eroded wall of Bowmans capsule; G= glomerulus; IPC= increased number of

podocytes; IMC= increased number of mesangial cells; OD= oedema; PC= podocytes; PT= proximal convoluted tubule; UP=urinary palp; VT= vacuolated tubule; WUS= widened urinary space.


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Plate 6: Transverse sections of kidney of Carbofuran treated mice after 25 days. Slides for the treatment groups (T1-T4) aredesignated by 6.1, 6.2, 6.3 and 6.4, respectively. Abbreviations: CDB= cell debris; CG= congested glomeruli; DCD= dilated

collecting duct; DG= degenerated glomeruli; DMR= dilated medullary ray; DT= dilated tubule; EWB= eroded wall ofBowmans capsule ; G= glomerulus; HA= hyalinized area; INF= inflammatory cell infiltration; IPC= increased number of

podocytes; OD= oedema; PT= proximal convoluted tubule; SG= shrinked glomeruli; VT= vacuolated tubule; WUS= widenedurinary space.

Plate 7: Transverse sections of kidney of Carbofuran treated mice after 35 days. Slides for the treatment groups (T1-T4) aredesignated by 7.1, 7.2, 7.3 and 7.4, respectively. Abbreviations: CG= congested glomeruli; DBC= degenerative Bowmans

capsule; DCD= dilated collecting duct; DDT= dilated distal tubule; DG= degerated glomeruli; DPT= dilated proximal tubule;DT= dilated tubule; G= glomeruli; HE= haemorrhage; IMC= increased number of mesengial cells; INF= inflammatory cell

infiltration; PT= proximal convoluted tubule; VT= vacuolated tubule; WUS= widened urinary space.


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Plate 8: Transverse sections of kidney of Carbofuran treated mice after 45 days. Slides for the treatment groups (T1-T4) aredesignated by 8.1, 8.2, 8.3 and 8.4, respectively. Abbreviations: CG= congested glomeruli; DCD= dilated collecting duct;

DG= degenerative glomeruli; DPT= dilated proximal tubule; DT= dilated tubule; EWB= eroded wall of Bowmans capsule;HE= haemorrhage; IMC= increased number of mesangial cells; IPC= increased number of podocytes; OD= oedema; PT=

proximal convoluted tubule; SPT= shrinked proximal tubule; VDT= vacuolated distal tubule; WUS= widened urinary space.

Oral administration of Dimethoate in albino miceat 7, 14 and 28 mg/kg body weight resulted inabnormal liver and kidney histopathology thatincluded hepatocytic pycnosis, vacuolization, bloodcongestion, high lymphatic infiltration around thecentral vein, enlargement of hepatic sinusoids,hepatocellular damage, necrosis, increase in thenumber of Kuffer cells, lesions and hemorrhage(Yasin and Sharma, 2013). Recently, El-bendary et al.(2014) evaluated histopathological abnormalitiesassociated with Profenofos and Chloropyrifosexposure in male albino mice where liver showedhepatic cell damage with degenerative changesincluding congestion of blood vessels, vacuolardegeneration of hepatic cells, focal infiltration andmononuclear cells, dilated central vein and otherhepatic blood vessels, necrosis of hepatic cells,disorganized with the formation of denoid structureand hepatocytomelagy; whereas kidney showedhemorrhage, oedema, necrosis and glomerularshrinkage. In addition, histopathological abnormalitiesin kidney cells included perivascular oedema withcongestion of renal blood vessels, infiltration ofmononuclear cells around glomerular tubules, oedemaof B owmans capsule and coagulation necrosis ofsome renal tubules. These results appear to fit wellwith those of the present investigation.

Being a broad spectrum carbamate pesticide,Carbofuran is extensively used against soil and foliar

pests of field, fruit, vegetables and forest crops, whichhas been reported to be highly toxic by inhalation andingestion, and moderately toxic by dermal absorption(WHO, 1985). It is highly toxic to aquatic biotaincluding fishes, environment as well as humans andis reported to propagate through oral and inhalationroutes of exposure (Baron, 1991). Moreover,environmental pollution and health hazards includingcases of severe, sub-severe and chronic human andwildlife poisoning through food chain or contaminatedfoods and drinking water have been reported (Aziz etal., 2008; Chowdhury et al., 2012). Because humansare at the top of the food chain, it is probable thatdetrimental residues of Carbofuran may remain in theedible portion of the vegetable or plants and thus mayaffect human health and well-beings. Several reportsdemonstrate that exposure of Carbofuran results insome histopathological changes in liver and kidney ofhuman and other mammals that include mononuclearcell infiltration, congestion, enlargement of the veinsand sinusoids, necrosis, increased number of Kupffercells, cytoplasmic vacuolation and degenerativehepatocytes (Aziz et al., 2008; El-Damaty et al.,2012). These are in good agreement with the presentresults on histopathological changes in theexperimental mice.


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Recent studies showed that indiscriminate andunregulated uses of insecticides like Carbofuran inagriculture and public health in Bangladesh have ledto drastic effects in many non-target species includingman (Chowdhury et al., 2012; Uddin, 2013). Since the

present feed treatments of albino mice withCarbofuran clearly demonstrated decrease in body,liver and kidney weights as well as marked changes inthe histopathology of hepatic and renal tissues, itcould be possible that prolonged exposure to thisinsecticide in man may play a significant role inaggravating such diseases as chronic liver and renalfailure. In addition, structural changes to hepatic andrenal tissues such as haemorrhage, congestion,vacuolation and erosion may also lead to acute liver orkidney damages and/or carcinogenicity of the organs.

The present results could thus be exploited as a potential biomarker of common insecticide toxicity inhuman beings.

5. CONCLUSION

The present findings clearly demonstrate thatCarbofuran is capable of inducing dose-dependentmorphometric i.e. body, liver and kidney weights andtheir relative weights as well as histopathologicalchanges in the liver and kidney of the exposed mice.According to these data, it is suggested that systemic

insecticide like Carbofuran exposure might causehazardous effects, especially at high doses, to man andenvironment. For field and domestic uses of thisinsecticide, quantities and mode of usage need to bestrictly monitored to minimize the possibility of itsexposure to non-target organisms including human

beings. This can be achieved through public healtheducation to make people aware of the hazardouseffects of this chemical. It is therefore recommendedthat great precautions are to be taken to minimize theharmful side effects of Carbofuran to the environment,especially to man, animals and agricultural products,aiming at avoiding environmental pollution.Moreover, recommended doses of the insecticide and

precautionary measures like wearing of impermeablegloves and masks to reduce the risk of inhalation ofspray should be implemented. Due attention also is to

be paid for a delayed period of field application of thisinsecticide to avoid its possible adverse effects toconsumers, who should be warned of the potential riskof Carbofuran contamination of food and drinkingwater in the country.

Acknowledgements

The authors are grateful to the Chairpersons,Departments of Zoology and Genetic Engineering &Biotechnology, University of Rajshahi, Bangladesh,

for providing laboratory facilities, and to LaboratoryAttendants, for their technical assistance. Sincerethanks must go to the anonymous reviewer for hisuseful comments and suggestions.

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Dr. M. Saiful Islam, Professor, Department of Zoology, University of Rajshahi, Rajshhai 6205,Bangladesh. The author was born on December 4, 1955 at Bogra, Bangladesh. He received his BScHonours (1977) and MSc (1978) Degrees in Zoology from the University of Rajshahi, Bangladesh,where he started his teaching and research career as a Lecturer in Zoology in 1983. Subsequently he had

his second MSc in Applied Entomology and Crop Protection from the University of Newcastle uponTyne, UK (1990), PhD in Insect Physiology and Behaviour from the Universities of Reading andOxford, UK (1995), Commonwealth Academic Fellowship in the Department of Zoology, University ofOxford, UK (2001-2002) and Visiting Fellowship in the Department of Entomology, University ofKentucky, USA (2003-2005). Meanwhile, Dr. Islam was promoted to Assistant Professor (1986),Associate Professor (1995) and Professor (1998) in his parent Department, where he is currently

employed. Professor Islam has supervised quite a good number of MSc thesis (>22) and PhD students (17) since 1983. He hasa credit of publishing over 120 research papers in renowned scientific journals of home and abroad. In addition, he co-authoreda couple of text books titled Biotechnology and Genetic Engineering and Introduction to Genetics while his another booknamed Genetics: The Science of Heredity and Variation is awaiting publication. Prof. Islam is a member of a large numberlearned bodies: Fellow of the Royal Entomological Society (FRES), London; Fellow of the Zoological Society of Bangladesh(ZSB); Life Member, Zoological Society of Bangladesh (Regional Secretary, 1996-1998); Life Member, Genetical Society ofBangladesh (Treasurer, 1999-2005); Life Member, Bangla Academy, Bangladesh; Life Member, Association of the

Bangladesh Commonwealth Scholars; Life Member, Bangladesh Entomological Society; Member, Bangladesh Association forthe Advancement of Science (BAAS); Member, Asiatic Society of Bangladesh and Ex-Member, American Association for theAdvancement of Science (AAAS). He has conducted research for a number of grants funded by various organizationsincluding the University of Rajshahi, Ministry of S & T, UGC of Bangladesh, TWAS (Italy) and IAEA (Austria). Prof. Islamserved as an Executive Editor and Editorial Board member of several scientific journals and periodicals. He teaches vertebrateand invertebrate Zoology, Microbiology, Biostatistics, Evolution, Embryology & Developmental Biology and AnimalBehaviour to undergraduate, and Genetics & Molecular Biology to postgraduate students. His current research interestincludes: Genetics and Molecular Biology of pest insects, inheritance of Mendelian and non-Mendelian traits in man, andapplications of breeding principles to farm animals. Email address: [email protected].

Dr. Moni Krishno Mohanta, Assistant Professor, Department of Zoology, University of Rajshahi,Rajshahi 6205, Bangladesh. Dr. Mohanta was born on March 4, 1979. He received his BSc inZoology (2001), MSc in Zoology (Genetics and Molecular Biology) in 2002 from the University ofRajshahi, Bangladesh and PhD in Environmental Microbiology from the same University in 2009.Presently he is working as an Assistant Professor in the Department of Zoology, Rajshahi University,Bangladesh. He has published a dozen of papers in different Journals. So far Dr. Mohanta hassupervised eight research students at BSc and MSc levels . He teaches Cell Biology, Paleontology andReproductive Biology to undergraduate and Microbial Genetics and Biotechnology to postgraduatestudents. His current research interest lies in the areas of Environmental Microbiology andToxicology. Email: [email protected]

Dr. Ananda Kumar Saha, Professor, Department of Zoology, University of Rajshahi, Rajshhai 6205,Bangladesh. Dr. Saha was born on October 31, 1957 at Magura, Bangladesh. He received his BScHonours (1979) and MSc (1980) Degrees in Zoology from the University of Rajshahi, Bangladesh,where he started his teaching and research career as a Lecturer in Zoology in 1987. Subsequently hehad his second MSc in Environmental Microbiology from the University of Newcastle upon Tyne,UK (1991), PhD in Microbiology from the University of Pune, India (2002). Presently he is workingas a Professor in the Department of Zoology, Rajshahi University, Bangladesh. Professor Saha hassupervised quite a good number of MSc thesis and PhD students. He has published over 40 research

papers in renowned scientific journals of home and abroad. Prof. Saha is a member of a large numberlearned bodies: Life Member, Zoological Society of Bangladesh (ZSB), Life Member, Genetical

Society of Bangladesh, Life Member, National Environmental Science Academy, India, Life Member, Biodiversity ResearchGroup of Bangladesh (BRGB), Life Member, Microbiological Society of Bangladesh, Member, Bangladesh Association forthe Advancement of Science (BAAS), Member, Asiatic Society of Bangladesh and Member, Microbiological Society of India.He teaches Cell Biology and Microbiology to undergraduate and Genetics & Molecular Biology to postgraduate students. Hiscurrent research interest lies in the areas of Environmental Microbiology, Waste water management and Toxicology. Emailaddress: [email protected].
mailto:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]:[email protected]


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Anup Mondol, Microbiologist, Mostofa Organic Shrimp Product Ltd., Satkhira, Khulna. Born on the15 th January, 1988, Gopalgonj, Bangladesh. Mr. Mondol received his BSc Honours (2009) and MSc

(2010) degrees in Zoology from University of Rajshahi, Bangladesh, in which he got First Class in both examinations. He has two years research experience during which he conducted hisundergraduate and graduate studies. He has developed good computer skills and has commendablelanguage proficiencies in Bengali, English. Email: [email protected]

Muhammad Mizanul Hoque, Assistant Officer, Islami Bank Bangladesh Limited, Natore. Born on the2nd of August, 1985, Mr. M. M. Hoque received his BSc Honours in Biotechnology & GeneticEngineering from K hulna University, Bangladesh in 2008. His masters thesis on Swiss albino mice

in the Department of Zoology, Rajshahi University, was highly commendable and he was awardedMS from his parent department in 2013. Owing to his extraordinary performance Mr. Hoque wasawarded Merit Scholarships three times during the academic sessions of 2005-2006, 2007-2008 and2009-2010. He is currently employed by the Islami Bank Bangladesh Limited where he is anAssistant Officer in ICT-based banking operations. Email: [email protected].

Dr. Apurba Kumar Roy, Associate Professor , Department of Genetic Engineering and Biotechnology ,University of Rajshahi , Rajshahi 6205, Bangladesh. Dr. Roy was born on the 17 th May, 1970 at

Narail, Bangladesh. He received his BSc (Honours) degree (1992) from the Department of Botany,Rajshahi University, Bangladesh. He received his MSc (1994) in the Department of Genetics andBreeding and PhD in Genetics in the same University where he started his research and teachingcareer as Lecturer. Currently he is an Associate Professor in the Department of Genetic Engineeringand Biotechnology. He teaches Fundamentals of Botany, Developmental Biology, Pathology, HumanGenetics, Immunogenetics, Food Biotechnology and Biomedical Science to undergraduate and

postgraduate students. His current research interest lies in the areas of Biomedical Science andToxicology. Email: [email protected].
mailto:[email protected]:[email protected]:[email protected]:[email protected]

Documents

Carbofuran-Induced Alterations in Body Morphometrics and Histopathology of Liver and Kidneys in the Swiss Albino Mice Mus Musculus L