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The association between hepatic microsomal enzyme induction and triacylglycerol metabolism was examined in fasting male guinea pigs injected intraperitoneally with 50 mg phenobarbital x kg-1 for 7 days. Enzyme induction was established by a significant increase in hepatic aminopyrine N-demethylase activity, cytochrome P450 content, and hepatic gamma-glutamyl-transferase activity. Increased activity of gamma-glutamyltransferase was also observed in the blood serum of treated animals. The phenobarbital-treated guinea pigs manifested increased hepatic triacylglycerol content and serum triacylglycerol concentration, accompanied by enhanced ability of cell-free fractions of liver to synthesize glycerolipids in vitro from sn-[14C]glycerol 3-phosphate and fatty acids. Microsomal phosphatidate phosphohydrolase accounted for 97% of the total liver activity of this enzyme, and its specific activity was 50-fold higher than that of the cytosolic enzyme when each was measured under optimal conditions. Activity of the cytosolic phosphohydrolase per liver doubled and that of the microsomal phosphohydrolase increased by 40% in the phenobarbital-treated guinea pigs. The microsomal, but not the cytosolic enzyme, showed a significant correlation with hepatic triacylglycerol content. Significant correlation was observed between the various parameters of hepatic microsomal enzyme induction and hepatic triacylglycerol content, suggesting that enzyme induction may promote triacylglycerol synthesis and consequent hypertriglyceridaemia in the guinea pig.

Background: Brain tumors are highly aggressive tumors characterized by secretions of high levels of matrix metalloproteinase-2 and -9, leading to tumor growth, invasion and metastasis by digesting the basement membrane and extracellular matrix components. We previously demonstrated the effectiveness of a nutrient mixture (NM) containing ascorbic acid, lysine, proline, and green tea extract in vitro: on activity of urokinase plasminogen activator, matrix metalloproteinases and TIMPs in various human glioblastoma (LN-18, T-98G and A-172) cell lines and on glioblastoma A-172 cell proliferation and Matrigel invasion. Aim: Our main objective in this study was to investigate the effect of the NM in vivo on human glioblastoma U-87 MG cell line. Materials and Methods: Athymic male nude mice inoculated with 3·106 U-87 MG cells subcutaneously and were fed a regular diet or a regular diet supplemented with 0.5% NM. Four weeks later, the mice were sacrificed, the tumors were weighed and measured. The samples were studied histologically. Results: NM inhibited tumor weight and tumor burden by 53% (p = 0.015) and 48% (p = 0.010), respectively. Conclusions: These results suggest the therapeutic potential of NM as an adjuvant in the treatment of glioblastoma.

Hepatic microsomal phosphatidate phosphohydrolase (PPH) showed minor fluctuations with age in male and female rats. In males, hepatic cytosolic PPH rose to a peak at day 58 and then declined. In female rats, the activities of this enzyme were much lower than those of the male to day 35, but then increased fivefold by day 50 to values approximating those of males, and thereafter gradually declined. The hepatic triacylglycerol (TG) content of male rats was fairly constant, but in females the values rose to a peak on day 50 and then declined in parallel with the cytosolic PPH activity, but remained substantially higher than values for male rats. A significant correlation between cytosolic PPH and hepatic TG was obtained. The microsomal PPH did not correlate with hepatic TG. These results suggest that in the rat cytosolic PPH may play a role in modulating age-related changes in hepatic TG metabolism, and that it is functionally more important than the microsomal enzyme in this species.