Fd Cosmrr. To.&. Vol. 20. pp. 137 10 147. 1982 Printed in Great Brilain

Information Section ABSTRACTS AND COMMENTS

Chromosome damage from caramel

Stich, H. F., Stich, W., Rosin, M. P. & Powrie, W. D. (1981). Clastogenic activity of caramel and carame- lized sugars. Mlrration Res. 91, 129.

Long-term feeding studies on various types of cara- mel have revealed no evidence of carcinogenicity, although ammonia-process caramel produced lym- phocytopenia at all levels tested (Evans et (11. Fd Cos- met. Toxicol. 1977, 15, 523). A food-grade caramel also gave negative results in an Ames test with five Salmonella strains (Bonin & Baker, Fd Technol. Aust. 1980, 32, 608). However, a very weak mutagenicity of caramel to S. ryphimurium TAlOO was reported else- where, and several other studies have demonstrated the mutagenicity of sugar pyrolysates (Sugimura et al. CRC Crit. Reo. Toxicol. 1979, 6, 189). A sugar-ammo- nia model system, the reaction products of which in- cluded many pyrazines, was also strongly mutagenic (Spingarn & Garvie, J. agric. Fd Chem. 1979, 27, 1319).

In the present study Chinese hamster ovary cells were exposed for 3 hr to commercial caramel powder (a positively-charged material prepared by heating a sugar-ammonium solution), or to caramelized sol- utions of sucrose, fructose, glucose, mannose, maltose or arabinose (prepared by heating solutions at 180°C for 1 hr). The caramel and all the caramelized sugars induced a high frequency of chromosome breaks and exchanges, the potency of caramel itself (which pro- duced 46% metaphase plates with chromosome aber- rations) being exceeded bnly by caramelized fructose. Non-caramelized sugars did not increase the aberra- tion frequency. The transition metals Cu2+ and Mn2+ had no effect on caramel’s potency, but Fe’+ and Fe’+ had a strong inhibitory effect. Addition of an S-9 microsomal preparation from PCB-pretreated rats abolished the clastogenic activity of the caramel powder, and this property was unimpaired by re- moval of NADP or MgClz from the S-9 mixture. However, heating for 20min at 80°C did destroy its inhibitory action. It was concluded that the effects of __ __.- _-_ _-. the S-9 preparation were not due to the mlxed-func- tion-oxidase system, but might result from a physical binding of caramel to S-9 components.

No attempt has yet been made to identify the clas- togenic ingredients of caramel, although possible can- didates may be furan and its derivatives or maltol. As yet unpublished studies by the authors have shown some of the former to be mutagenic in more than one test system, while the latter induced reverse mutations in S. typhimurium strain TAlOO (Bjeldanes & Chew, Mutation Res. 1979, 67, 367).

[Whether these in cicro findings have any signifi- cance to caramel consumption by man is still open to question. If its potency is abolished by binding to S-9 components, it may similarly be abolished by binding to dietary components.]

0278.69lS/82/OlOl37-I 1SO3.00/0 Pcrgamon Press Ltd

Yet more coffee-drinking rats

Nolen, G. A. (1981). The effect of brewed and instant coffee on reproduction and teratogenesis in the rat. Toxic. appl. Pharmac. 58, 171.

There have recently been a number of reports on the hazards linked with caffeine and its associated drinks. In the last issue (Cited in F.C.T. 1981, 19, 789) we reported a paper linking coffee with pancreatic cancer and earlier we detailed studies that indicated possible teratogenic effects in the rat (Food Chemical News 1980, 22, (26). 35; Cited in F.C.T. 1981. 19, 510). We have previously commented (ibid 1981, 19, 510) that care should be taken in drawing conclusions from these studies since it is possible that the rat is uniquely unable to cope with caffeine stress. It is, therefore, rather disappointing to find yet another study using the same species and providing little extra information.

Brewed or instant coRee containing at full strength 0.057 and 0.045% caffeine, respectively, was given to groups of 20 male and 30 female rats in place of their drinking-water either at full strength or as 50 or 25% dilutions. Control animals received distilled water. Administration continued f&r about j0 wk, from weaning through two pregnancies. The initial mean daily caffeine intakes of the females were 181, 98 and 57mg/kg body weight in the high-, medium- or low- dose brewed coffee groups, respectively, and 148, 81 and 45 mg/kg, respectively in the groups given instant coffee. During lactation the daily caffeine intakes were 97. 53 and 30 mg/kg in the rats given brewed coffee and 80,46 and 22 mg/kg in those given instant coffee. Ten animals from each group were killed at 13 wk and examined. The remaining rats were mated and the resulting pups were culled to eight/litter. Ten days after their first litter had been weaned the females were mated again and killed at either day 13 or 21 of pregnancy. The pups in the first litter were weighed and then discarded when 21 days old. The foetuses from the second mating were examined. for any ab- normalities.

Rats given full-strength coffee tended to drink less than those given the diluted brew but all the coffee- drinkers grew as well as or better than the controls. All of the rats given 100% instant or brewed coffee solutions had enlarged kidneys at 13 and 30 wk but at the 50% dilution only the females showed any kidney enlargement. The females were also more susceptible with regard to their livers, full-strength coffee produc- ing an enlargement at both 13 and 30 wk in females but not in males, and 50% coffee solution producing this effect in females at 13 wk. No effects on organ weights were seen in the low-dose group.

No effects of coffee ingestion on reproduction or lactation were observed except for a significant reduc- tion in the body weights at weaning of the pups of dams eiven lOOo/:, coffee solution. Neither were any

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138 Food additives and contaminants-Fd Chem. Toxic. Vol. 20. No. I

embryotoxic or teratogenic effects noted even in the groups given the full-strength cotfee which provided caffeine intake equivalent to that (80mg/kg body weight) at which ectrodactyly (missing toes) occurred in an FDA study (Food Chemical News 1980, 22, (26) 35). However, delayed ossification of the sternebrae was noted, but only in the groups given 100 or 50% brewed coffee solutions or lOO”/, instant coffee sol- ution. In the FDA study this effect occurred even at the lowest dose level of 6 mg caffeine/kg.

[In the FDA study (Food Chemical News 1980, 22 (26). 35) the caffeine solutions were administered by gavage. A recent study using [t4C]caffeine has indi- cated differences in blood levels of caffeine and in the relative distribution of 14C in the blood and placenta between rats given caffeine solution by gavage and those sipping the solution (Food Chemical News 1981. 23 (91 32). Differences in dosing methods may there- fore explain some of the differences in the results of the two studies mentioned above.]

Living it up on Watership Down

Klurfeld. D. M. & Kritchevsky, D. (1981). Differential effects of alcoholic beverages on experimental ather- osclerosis in rabbits. Expl tnolec. Par/~. 34, 62.

The debate on the possible health benefits of a moderate intake of alcohol needs little introduction. The arguments have continued for a long time. col- oured not a little by the conflict between the view that “a little of what you fancy does you good” and the more puritanical assumption that if it’s enjoyable it must be bad-in one sense or another. While there is no doubt about the adverse effects of high intakes of ethanol in any form, claims for the health-promoting effects of moderate drinking make the news from time to time (Cired in F.C.T. 1981, 19, 789) and diver- gent assertions on the relative merits of various types of alcoholic beverage as a protection against coronary heart disease led the authors cited above to study the relationship between alcohol consumption and athero- genesis in animals.

The study they describe compared the effects of a moderate intake of various alcoholic drinks on the development of atherosclerosis in rabbits fed a semi- purified diet, which was formulated to simulate “the average American diet” and was supplemented with additives to meet the rabbit’s nutritional needs and with sufficient cholesterol (0.5”:) to induce athero- sclerosis rapidly. Groups of eight rabbits were fed this diet for 3 months together with one of the following drinking fluids: 12.5”,, glucose in water (control group). red wine. white wine, bourbon whiskey, beer or ethanol in water. The beer contained 4.9”,; ethanol: the other fluids were diluted to 9.5”, ethanol. At the end of the treatment. and after an overnight fast. the animals were killed for blood studies and histopatho- logy. Fluid consumption. recorded daily, was signifi- cantly below the control intake in all the test groups except that given beer (33-46 ml/day for the test groups ~7. 73 ml/day for the controls). Weight loss in all the animals, including the controls, was attributed to the relative unpalatability of the diet although the weight loss in the red-wine and white-wine groups

was significantly greater than that in the control group. Total serum lipids were similar in all the groups.

None of the ethanolic fluids caused liver enlarge- ment or exacerbated the hepatic-lipid accumulation caused by the diet. Hepatic levels of cholesteryl esters were actually lower in the treated groups than in the controls. Again in comparison with the controls, both aortic and coronary atherosclerosis were considerably reduced by consumption of red wine and showed some reduction in the groups given ethanol-water, white wine or whiskey, but beer was ineffective in this respect. The aortic lesions were of two types: fatty streaks composed almost entirely of foam cells, and a more advanced type of atheroma characterized by proliferation of smooth muscle cells in a loose col- lagenous matrix. Some animals (about 20%) had both types of lesions, but the former type was more com- mon in the control and red-wine groups and the latter predominated in the other test groups. Analyses of serum and liver for high- and low-density lipoprotein (HDL and LDL), showed that HDL-cholesterol and HDL-phospholipid concentrations were greatly increased by all the alcoholic fluids except beer. Con- sequently there were significant reductions in LDL/HDL ratios and a marked increase in the per- centage of total cholesterol contributed by HDL. Dis- cussing this the authors refer to evidence that levels of HDL cholesterol may be inversely related to mor- bidity and mortality from coronary heart disease.

While the mechanisms underlying these findings require further investigation, this study provides sup- port for the view that the consumption of alcoholic beverages is not atherogenic and may exert a protec- tive effect. The varying effects of the different types of beverage indicate the involvement of constituents other than ethanol in the overall response.

The effects of dietary cyanide

Tewe, 0. 0. & Maner, J. H. (1981). Long-term and carry-over effect of dietary inorganic cyanide (KCN) in the life cycle performance and metabolism of rats. Toxic. appl. Phurmtrc. 58, I.

Chronic cassava consumption by malnourished human populations is associated with a distinctive clinical syndrome. which includes degenerative neuro- logical disease and endemic goitre (Cired in F.C.T. 1980. 18, 445). These effects are caused by cyanogenic glycosides such as linamarin, present in the cassava and hydrolysed in cico to cyanide. coupled with chro- nic nutritional deficiency. The latter factor may involve shortages of sulphur-containing amino acids. which normally assist the enzyme rhodanase in detox- ifying cyanide, and/or vitamin Blz (ibid 1970,8, 606 & 711; ibid 1975, 13, 157). No thyroid lesions were ob- served in rats fed nutritionally-balanced fresh cassava diets containing 196 ppm hydrocyanic acid for 4 months (Maner & Gomez, in Chronic Cossaca Toxi- city: Proceedings oj an Interdisciplinary Workshop, London, 1973: Int. Devel. Res. Centre Monogr. IDRC-OlOe. 1973. p. 113). However, the same authors showed that 480ppm cyanide (as KCN) reduced rat growth and feed consumption. and at 960 ppm some