Food and cosmetics toxicology最新文献

Peanut oils obtained from Hong Kong markets were frequently contaminated with aflatoxins. A ‘purified’ diet in which aflatoxin-contaminated market peanut oil (aflatoxin B₁ 110 ppb [μg/kg]) was used as the fat source was fed to Sprague-Dawley rats for 22 months from weaning. Its estimated aflatoxin B₁ content was 5–7 ppb. Controls were fed a diet of identical composition except that Mazola corn oil (aflatoxin-free) was used. At autopsy, three out of 76 aflatoxin-fed rats were found to have sarcomas—one in the liver, one in the wall of the colon and one in the subcutaneous tissue of the groin. Eighteen animals fed peanut oil showed parenchymal liver damage and varying degrees of fatty change and one showed pre-malignant changes in liver cells. Of 90 control rats, none developed malignant tumours. The liver-to-body weight ratios for experimental and control rats were 2·93 ± 0·46 and 2·62 ± 0·58, respectively (means ± 1 SD). The difference between these values was statistically significant (P < 0·01), reflecting the degree of fatty change in the livers of experimental rats compared with that in the controls. Over 90% of Hong Kong households use peanut oils for cooking purposes, and these data appear to indicate a possible health hazard in the use of peanut oils contaminated at the levels found.

This work was undertaken to determine whether or not propyl gallate, added as a 0·3% (w/w) supplement to purified diets containing various types and amounts of fat, modifies the function of the hepatic microsomal mixed-function oxidase system. The criteria used included measurements of liver weight, liver to body-weight ratio and hepatic microsomal-protein level as well as analyses of specific components and functions, such as total microsomal cytochrome P-450 content, and the levels of activity of aniline hydroxylase, aminopyrine N-demethylase and NADPH-cytochrome c (P-450) reductase. In contrast to butylated hydroxytoluene, propyl gallate at a level of 0·3% in the diet did not alter the function of the mixed-function oxidase system, even when administered in a diet high in polyunsaturated fat, which has a permissive effect on the induction of hepatic cytochrome P-450 levels by phenobarbital and 3-methylcholanthrene.

Sodium o-phenylphenate (OPP-Na), a fungicide approved as a food additive in Japan, was given in pellet diets at dietary levels of 0, 0·125, 0·25, 0·5, 1·0, 2·0 or 4·0% to groups of about 10 male and female F344/Du rats for 13 wk and to male F344/Du rats for 91 wk. In the 13-wk study, urinary bladder tumours developed in one out of ten male rats fed 1% OPP-Na, nine out of ten male rats fed 2% OPP-Na, one out of ten male rats fed 4% OPP-Na and two out of ten female rats fed 4% OPP-Na. Five transitional cell carcinomas were observed in male rats fed 2% OPP-Na and one such carcinoma was found in a male rat fed 4% OPP-Na. In the 91-wk study, tumours of the urinary bladder, renal pelvis and renal papilla developed in one out of 21 rats (5%) fed 0·5% OPP-Na, seven out of 21 rats (33%) fed 1% OPP-Na, 20 out of 21 rats (95%) fed 2% OPP-Na and 17 out of 21 rats (85%) fed 4% OPP-Na. These were all transitional cell carcinomas, except for one carcinosarcoma in the 2% group. A dose-related increase in the incidence of non-neoplastic lesions of the kidney were observed in treated rats. In the 13-wk study, slight to moderate pyelonephritis was observed in six out of ten male rats and one out of ten female rats fed 4% OPP-Na. In the 91-wk study, moderate to severe pyelonephritis was observed in four out of 21 rats (19%) fed 2% OPP-Na and in all of 20 rats fed 4% OPP-Na.

The metabolism of zearalenone in the urine of the cow, the pig, the rabbit, the rat and man was studied. Both free and conjugated zearalenone (63%), α-zearalenol (32%) and β-zearalenol (5%) were present in the urine of the pig; α-zearalenol was the predominant metabolized species. In the cow, free and conjugated (glucuronic and sulphate) zearalenone (29%), α-zearalenol (20%) and β-zearalenol (51%) were found; in contrast to swine, β-zearalenol was the predominant species. In rat urine, the major species was free zearalenone, which constituted over 90% of the total zearalenone and metabolites. In the rabbit, 46% of the urinary metabolites took the form of zearalenone conjugates, 29% were conjugates of α-zearalenol and 25% were conjugates of β-zearalenol. The distribution of metabolites in the faeces was similar to that in the urine. In man, zearalenone and α-zearalenol were the major metabolites followed by β-zearalenol; all were in the glucuronide form.

Free and conjugated forms of zearalenone and diastereomeric zearalenols were present in cows' milk. The total concentration of zearalenone and its metabolites was 1·3 ppm (after receiving 25 ppm dietary zearalenone for 7 days); zearalenone constituted 35%, α-zearalenol, 31% and β-zearalenol, 34% of the free metabolites. α-Zearalenol is three times more oestrogenic than zearalenone.

2,3,7,8-Tetrachlorodibenzofuran (TCDF) at levels of 50 and 5 μg/kg (ppb) in food caused sickness and some deaths in groups of three rhesus macaques fed for 2 months and 6 months, respectively. The principal pathological changes were atrophy or squamous metaplasia of the sebaceous glands, mucous metaplasia and hyperplasia of the gastric mucosa; involution of the thymus and hypoplasia of the bone marrow. In animals that did not die during the experimental feeding, recovery was complete after 3 months of a TCDF-free diet.