Cholesterol HDL in G-6-PD deficient newborn infants following phenobarbital administration.
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Biomedical subjects
Publications and source records attributed to P Pani.
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Acute toxicity induced by DMN was partially prevented by previously administering methyl mercuric chloride (MMC), a chemical inhibitor of the drug metabolizing enzyme system (DMES). We have studied the early changes occurring during the course of DMN-intoxication, namely disaggregation of polysomal profiles and necrosis, evaluated morphologically and by the release of S-GPT.
The effect of lead nitrate, an inhibitor of the hepatic drug-metabolizing enzyme system upon the acute, hepatotoxicity of dimethylnitrosamine (DMN) was studied. Lead pretreatment significantly prevented polysomal disaggregation induced by the nitrosamine. Cell necrosis, evaluated morphologically and by the release of serum glutamic-pyruvic transaminase (GPT), was also diminished. The metabolism of DMN in rats pretreated with lead nitrate was investigated by following its clearance from blood and by determining, in vitro the demethylation of the nitrosamine. Lead increased, although not significantly, the clearance of DMN from blood, but it lowered the activity of DMN-demethylase 24 h after its administration. Finally, lead lowered the lethal effects of DMN. The mechanism by which lead influenced DMN toxicity is discussed.
Male rats were immunized against bovine albumin injected by either intradermic or intralymphatic routes. A significantly higher number of animals treated by the latter route did respond, probably because antigens introduced by this route directly reach lymph nodes, by passing blood and tissue lytic enzymes.
Tumor growth and survival time were followed in rats transplanted with Morris hepatoma 5123 and previously injected with a crude homogenate of the same tumor by the intradermic or intralymphatic route. Female rats treated by the intralymphatic route showed a longer survival time and impaired tumor growth. Male rats did not show any difference.
Pretreatment of rats with cerium chloride, an inhibitor of the DMES, protect against CCl4 intoxication. The protection was obtained against the fatty infiltration in the liver, the decrease of triglyceride secretion from the liver into the plasma compartment, the polysomal disaggregation and the rise of serum transaminases.
Most the lymphatic system in the rat was directly observed in our experiment by radiological means. The lymphatics of the limbs were firstly revealed by subcutaneous injection of Patent Blue V. Lipiodol was used as radio-opaque compound injected by a micro-technique fully described by the authors.
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After intravenous injection of palmitate-1-(14)C to rats fed a choline-deficient (CD) or choline-supplemented (CS) diet for 15-18 hr, liver triglycerides became labeled very rapidly. In CS, but not in CD rats, there was a considerable loss, with time, of radioactivity from liver triglycerides. At the same time, significantly less radioactivity appeared in plasma triglycerides of CD rats than of CS animals. No difference was seen in the triglyceride content of microsomes isolated from the liver of rats fed the two diets. The lower radioactivity in plasma triglycerides of CD rats was essentially due to a lower level and specific activity of very low density lipoprotein triglycerides. After intravenous injection of Triton and labeled palmitate, considerably less radioactivity accumulated in plasma triglycerides and phospholipids of CD rats than of CS animals. Post-Triton hyperphospholipidemia was also less pronounced in CD rats. It was concluded that the fatty liver observed in CD rats results from an impaired release of hepatic triglycerides into plasma.
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