The influence of acute poisoning with Dursban (O.P.I.) and D.D.T. (O.cl.I.) on serum enzymes and histopathological examination of the liver, kidney and testes was investigated in albino rats. Two repeated i.p. injections of Dursban in a dose of half the LD 50 resulted in a significant increase in serum GOT, GPT and alkaline phosphatase activity and a decrease of cholinesterase. In case of DDT, two doses of 150 mg/kg orally resulted in a significant increase in the activity of serum GPT only, while three doses increased serum GOT and GPT. No significant change was observed in serum alkaline phosphatase and cholinesterase activity. Regarding the pathological examination it was found that in animals treated with Dursban there was liver necrosis of mid-zonal type and fatty change at the periphery. In case of DDT the liver cells lost their radial arrangements and showed fatty change. There was cellular infiltration in the centre, mostly mononucleolar cells. In both insecticides there was necrosis of some of the seminiferous tubules of the testes and cloudy swelling of the convoluted tubules of the kidney. Histochemical study of the liver in animals treated with Dursban showed that glycogen was deposited at one side of the cell. However, there was depletion of glycogen around the central vein. In liver treated with DDT there were large globules of fat inside the liver cells, indicating increased fat content compared to control liver, where there were tiny minute droplets of fat.
In a group of Egyptian lead tank welders who were exposed to lead fumes for periods to 22 years the changes in serum lipids and some of the liver function tests which may elucidate the effect of lead on the liver were investigated. The results revealed increased blood lead level associated with decreased blood haemoglobin and increased urinary excretion of delta amino levulinic acid. However, no clinical abnormalities were recorded in the exposed group of the present work. Thus the increase in serum triglycerides and B-lipoprotein together with the lowering of the phospholipid/cholesterol ratio which were found may indicate premature development of atherosclerosis. Indirect evidence of the beginning of liver fattening was also provided by the increase in serum GOT, GPT, LDH enzymes and decreased albumin/globulin ratio besides the changes in serum lipid values. It is concluded therefore that lead poisoning may have a vascular as well as hepato-toxic action.
Carbon tetrachloride twenty-four hours after its administration resulted in a significant increase in serum iron, copper, zinc, calcium, potassium and sodium, while for magnesium no significant change was observed. A portion of this rise was due to the known hepatotoxic effect of CCl4 on the liver. Pretreatment with adenosine-5-monophosphate led to a normalization of the level of serum iron, copper and zinc, while in case of calcium, magnesium, potassium and sodium there was no significant change from that found in CCl4. The normalization of serum copper and iron under the influence of AMP may be due to some protective action of AMP on the liver. However, the disturbance in minerals metabolism may be considered as one of the earliest lesions in CCl4 poisoning.
The effect of vitamin B12 on the metabolic alterations due to tetracycline toxicity was studied experimentally on laboratory animals. Treatment of Sprague-Dawley rats with 120 or 250 mg tetracycline (i.p.) per kg per day for two or three days caused an accumulation of lipids, mainly triglycerides in the liver of 75% of animals studied, while phospholipid level tend to decrease. These doses are approximately twice and four times the recommended maximum dose for man. In the present work no direct relationship was observed between dose of tetracycline and hepatic accumulation of triglyceride, although livers of rats treated with 250 mg tetracycline/kg appeared uniformly pale yellow. Elevated serum triglyceride was found predominantly in rats treated with 120 mg/kg, while there was no obvious difference between serum triglyceride of rats treated with 250 mg tetracycline and control rats, indicating a block in the release of hepatic triglycerides. Where protection by vitamin B12 was studied, the vitamin was given i.m. (50 microgram/animal) 3 hours before the injection of 120 mg tetracycline per kg. There was a good evidence that lipid abnormalities caused by tetracycline improved by vitamin B12. Thus both hepatic and serum total lipid and triglycerides were significantly lower than those of rats treated with tetracycline, although hepatic total cholesterol was significantly increased as in case of tetracycline only.
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