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Biomedical subjects

D S Sarma

Publications and source records attributed to D S Sarma.

At least 109 records · Page 6Linked to original sources
PubMed1979

Persistence of DNA damage during development of liver angiosarcoma in rats fed dimethylnitrosamine.

Chronic feeding of a diet containing dimethylnitrosamine (50 ppm) to rats resulted in liver DNA damage monitored as slow sedimentation of the DNA compared to that of the control in alkaline sucrose gradients. The damage in rat liver DNA could be seen within 2 days after beginning the feeding of diets containing the carcinogen and was progressive with the time of feeding, up to 8 weeks. Extended feeding up to 15 or 31 weeks did not result in a proportionate increase in the damage to the DNA. The DNA damage observed at 8 weeks persisted until 31 weeks, at which time liver angiosarcoma was present. Despite the fact that the DNA damage induced by dimethylnitrosamine appears to involve the bulk of the liver DNA, the tumors developed were entirely from vascular endothelium. The implication of these results in the initiation of carcinogenesis is discussed.

Animals↗
PubMed1977

Effect of aflatoxin B1 on hepatic polyribosomes and protein synthesis in the rat.

This study was concerned with the effect of aflatoxin B1 on protein synthesis in rat liver. Specifically, the effect of the administration of aflatoxin B1 (6.0 mg/kg body weight) on hepatic polyribosomes (free and membranebound), protein synthesis in vitro, and initiation factors activity of rats within 3-12 h was investigated. The results revealed that aflatoxin B1 rapidly led to disaggregation of free and membrane-bound polyribosomes, to inhibition of in vitro protein synthesis by both populations of polyribosomes, to little or no effect on the activities of initiation factors, and to defective ribosomes, particularly the 60S ribosomal subnits, of both types of polyribosomes. Comparative studies on the effects of aflatoxin B1 and actinomycin D revealed progressive disaggregation by both hepatic free and membrane-bound polyribosomes after aflatoxin B1 but not only of the free polyribosomes after actinomycin D.

Aflatoxins↗
PubMed1977

Inhibition of dimethylnitrosamine-induced strand breaks in liver DNA and liver cell necrosis by diethyldithiocarbamate.

Diethyldithiocarbamate (DEDTC) prevented dimethylnitrosamine (DMN)-induced strand breaks in liver DNA and liver cell necrosis in male Wistar rats. In contrast, DEDTC did not inhibit the fragmentation of liver DNA caused by several other chemical carcinogens (N-hydroxy-2-acetylaminofluorene, 3-hydroxyxanthine, aflatoxin B1, N-acetoxy-2-acetylaminofluorene, methyl methanesulfonate, methylnitrosourea, and methylazoxy-methanol acetate), whether or not they required metabolic activation. Aminoacetonitrile exerted an action similar to that of DEDTC. The inhibitory effect was transitory, lasting at least for 4 hours, and protection for longer than 4 hours required multiple administrations of DEDTC. DEDTC also inhibited the serum clearance of DMN, methylation of liver DNA, and oxidative demethylation of DMN in the in vitro hepatic microsomal system prepared from either male Wistar rats or from hamsters. Interference of the metabolism of DMN appeared to be the mechanism by which DEDTC arrested DMN-induced biochemical and biologic effects.

Aminoacetonitrile↗
PubMed1976

Physicochemical alterations in the conformation of rat liver chromatin induced by carcinogens in vivo.

Administration of methylating carcinogens such as methyl methanesulfonate (120 mg/kg), dimethylnitrosamine (5 mg/kg), or methylnitrosourea (80 mg/kg) to rats resulted in an increased ellipticity in circular dichroism spectra and in an enhanced ability to bind ethidium bromide in the liver chromatin. Although shearing of the chromatin preparations increased both the ellipticity and number of binding sites for ethidium bromide, the carcinogen-induced effects were noticeable whether or not chromatin was sheared. Although the doses of the 3 carcinogens used in these studies are equivalent in their ability to induce strand breaks in liver DNA at 4 hr, their effects on the induction of conformational changes in liver chromatin are different. For example, methyl methanesulfonate induced the minimum conformational changes in liver chromatin at 4 hr, whereas methylnitrosourea induced the maximum changes at 4 hr. Methyl methanesulfonate and dimethylnitrosamine, on the other hand, induced maximum changes at 3 days. The conformational changes induced by methyl methanesulfonate and methylnitrosourea, and not by dimethylnitrosamine, tend to be repaired by 14 days.

Animals↗