Hepatic changes associated with chronic alcoholism in rats.
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Alcoholism↗
Biomedical subjects
E A Porta
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Chronic alcoholism enhances hepatocarcinogenicity of diethylnitrosamine in rats fed a marginally methyl-deficient diet.
To determine whether the chronic consumption of ethanol was capable of enhancing the hepatocarcinogenic activity of diethylnitrosamine per se, or through the accentuation of a methyl deficiency, two groups (A and B) of Sprague-Dawley female rats were fed for 10 months either a 20% casein basal diet marginally deficient in methyl, or the same diet supplemented with choline (1 gm per 100 gm) and folic acid (0.54 mg per 100 gm). Both groups were offered a drinking ethanol solution, while two other nonalcohol control groups (C and D) were isocalorically pair-fed to Groups A and B, and received diets in which the alcohol consumed by the corresponding groups was replaced by isocaloric amounts of sucrose. A baseline nonalcohol Group E, isocalorically pair-fed to Group A, received the intact basal diet of Group A and water. One day before the initiation of the experiment, and again 2 months later, all rats from the five groups were injected with a single i.p. dose of diethylnitrosamine (100 mg per kg). The growth attained by all groups was statistically similar. Hepatic triglycerides in Group A were significantly higher than in all the other groups. While in Group A primary hepatocellular carcinomas and renal tumors were encountered at the end of the experiment in 3 of 6 and in 2 of 6 rats, respectively, no malignancies were observed in any of the other groups. These results indicate that chronic ethanol consumption enhances the hepatocarcinogenic and renal tumorigenic activity of diethylnitrosamine, and strongly suggest that this action is mediated through the accentuation of methyl deficiency.
Alcoholism↗
Effects of dietary selenium on hepatic and renal tumorigenesis induced in rats by diethylnitrosamine.
Seven groups of female Sprague-Dawley rats (approximately 200 gm initial body weight) were injected i.p. with a single subcarcinogenic dose of diethylnitrosamine (40 mg per kg body weight) between 8 to 10 hr after partial hepatectomy, and after a recovery period of 3 weeks (herein called induction stage) received 0.05% phenobarbital in the diet for the rest of the experiment (promotion stage). The rats were fed a 20% casein-based diet containing 0.16 ppm of selenium or the same diet supplemented with 4 or 6 ppm of selenium as sodium selenite. The effects of these three dietary regimens were tested when administered 9 to 11 days before and during induction, 1 week before and during promotion or during the entire experiment. Pair-feeding conditions were used to minimize influences due to differences in food intake and growth. Despite similarities in food intakes, the growth rates in groups receiving the 6 ppm-selenium diet during promotion or during the entire experiment were in general significantly lower than in rats fed the 4 ppm-selenium diet or the 0.16 ppm-selenium basal diet. Survival rates were also significantly reduced in rats fed the 4 and 6 ppm-selenium diets during promotion or during the entire experiment. In rats killed at the 19th week for interim assessment of the experiment's progress, the stereologically analyzed numerical and volumetric densities of hepatic premalignant hyperplastic nodules did not differ significantly between groups. All the remaining rats were killed at the 46th week.(ABSTRACT TRUNCATED AT 250 WORDS)
Animal Feed↗
Advances in age pigment research.
Although it is presently accepted that lipofuscin (age-pigment) is the end product of the physiological decay of the cells' own constituents, the intimate mechanisms involved in its formation are largely unknown. The advances in the field of lipofuscinogenesis have been relatively slow, mainly due to the persistent confusion between the naturally occurring normal lipofuscin and the pathologically formed ceroid pigments. Therefore, attempts have been made in this presentation to review first the differential features between these pigments and second, to provide a general overview on the physicochemical properties of lipofuscin. The two prevailing theories on lipofuscinogenesis, the peroxidative theory and the proteolytic decline theory, are critically discussed, and future lines of research are suggested for the resolution of present uncertainties on lipofuscinogenesis. Since lipofuscin is properly considered the hallmark of cellular aging, it is expected that the unraveling of the mechanisms involved in lipofuscin formation will provide important clues to the still unknown underlying causes of cellular aging.
Journal Article↗