No abstract

The frequency of his+ revertants induced by N-methyl-N-nitrosourea (MNU) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the strain TA100 of Salmonella typhimurium was decreased by gallic and tannic acid. In weak buffer solutions, the inhibition effects of gallic acid towards MNU and MNNG mutagenicity was caused primarily by a decrease of pH in the incubation mixtures. At adjusted pH (pH 5.0 and 6.5), the antimutagenic effects are largely the result of an interaction between MNU or MNNG with phenolic acids outside the cells.

No abstract

In this study it was demonstrated that comprable doses of streptozotocin and alloxan produced similar degrees of pancreatic insulin depletion 48 hours after intravenous injection into rate. The metabolic status of animals injected with either streptozotocin (65mg/kg) or alloxan (60 mgfkg) was asseased prior to and 24 and 48 hours after injection. Metabolic changes consistent with the induction of acute diabetes were observed after both agents. N o qualitative differences were revealed between the responses to the two drugs as reflected by plasma glucose, FFA, glycerol and triglyceride response% and by changes in FFA and glycerol release in vitro. This applied whether the animals were fed ad libitum or were restricted to glucose as the sole caloric source.These results indicate that potential extrapancreatic toxic effects of alloxan and streptozotocin do not sigmficantly interfere with the acute diabetic metabolic changes induced by t h m agente and that these changes, over the first 48 hours, were primarily a consequence of /?-cell destruction and insulin deficiency. -Comparison of the effects of the differing dietary regimes indicates that both endogenous and exogenous triglyceride contribute to the hypertriglyceridaemia of the acute diabetes induced by both agents. Higher plasma triglyceride concentrations w-ere observed in streptozotocin than in alloxan treated animals fed a free diet but this difference ww not evident when the diet was replaced by glucose. Such quantitative differences in the metabolic responses to the two agents could be e.xplained on the basis of the observed variation in the rate of pancreatic insulin depletion and/or variations in food intake.

No abstract