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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.

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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.

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The intravenous injection of zinc or manganese chloride immediately before and 15 minutes after alloxan or dithizone prevented the usual hyperglycemia observed 24 hours after induction of diabetes. Injection of zinc chloride in alloxan diabetes led to normalization of sodium while zinc, copper, iron and magnesium remained high and calcium and potassium remained low as in alloxan. In case of dithizone diabetes, the administration of zinc salt led to an increase in serum zinc, magnesium and potassium and to a decrease in serum calcium while the sodium level returned to normal. Manganese plus alloxan led to a normalization of serum zinc, copper, potassium and sodium. In the case of dithizone plus manganese only magnesium was raised while the other elements were unchanged when compared to animals injected with dithizone only. Chromium and cobalt lowered the blood glucose to a certain extent however it did not affect most of the elements. The same changes occurred in all elements as with alloxan or dithizone alone. Pretreatment with ATP led to a normalization of serum zinc, copper, magnesium, sodium and potassium, while in case of iron it remained high and calcium remained low as that found in alloxan diabetic rats.

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The effect of ten repeated doses of carbon tetrachloride, phenobarbitone and propionyl promazine when administered alone or simultaneously with CCl4 on serum minerals was investigated. Carbon tetrachloride resulted in a significant increase in serum iron, copper, zinc, calcium, potassium and sodium. A portion of this rise was due to increased permeability in damaged mitochondrial membrane as a result of the action of CCl4. Propionyl promazine when administered alone or together with CCl4 has no effect on serum minerals. Phenobarbitone when administered alone increased serum minerals except sodium, but to a lesser degree than CCl4, while phenobarbitone when given repeatedly together with small doses of CCl4 led to a normalization of serum iron, calcium and potassium. Also serum zinc and copper were lower than in case of CCl4. This may be due to some protective effect of phenobarbitone on liver mitochondria. Serum magnesium was not affected in all the experimental groups.

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The influence of phenobarbitone givenin ten repeated doses simultaneously with small doses of CCl4 on serum enzymes was investigated in albino rats. The same experiment was repeated to investigate the influence of propionyl-promazine (phenothiazine derivative). The results proved that SGPT is a more specific and sensitive index than SGOT of hepato-cellular injury. The activity ratio between serum GOT and GPT in the normal control group was 2.44. The activity of SGPT increased nearly 6.1 fold after CCl4 administration and thus the activity ratio between GOT and GPT is sharply reduced to 0.56. The activity of serum GPT when CCl4 and phenobarbitone were administered together showed value of about 1/2 of the value when CCl4 was administered alone, while it remained high when CCl4 administration was combined with propionyl-promazine. Serum GOT and alkaline phosphatase increased significantly in all the groups. Regarding the pathological examination of the liver it was found that marked fatty necrosis could be demonstrated when high values of SGPT was found, which is not the case with serum GOT. It is concluded that in the present experimental conditions phenobarbitone protected the liver from the hepatotoxic effect of CCl4, while propionyl-promazine did not.

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In maturity onset diabetes the blood levels of total blood keto acids in terms of pyruvic, serum citric, calcium are significantly higher than in normal adults, while there is a decrease in reduced-blood glutathione, serum zinc, potassium and sodium levels. There were no significant differences between diabetes and normal adults in the serum levels of copper, ceruloplasmin oxidase activity, iron and magnesium.

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In cases of juvenile diabetes, there were lower than normal levels of reduced glutathione, ceruloplasmin oxidase activity, zinc, copper and sodium, while the other elements show no significant changes. The lower level of serum zinc, copper and sodium may be due to the osmotic diuresis and consequent polyurea of diabetes.

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Toxic metals encountered industrially or environmentally may produce the following syndromes: 1) Peripheral neuropathy: which is mainly sensory in arsenic and entirely motor with inorganic lead, organophosphorus compounds and tallium produce a mixed form of peripheral neuropathy. 2) Encephalopathy: usually with lead poisoning where ataxia and hemiplegia or optic atrophy may occur. 3) Optic neuritis: transient or permanent impairment of vision in arsenic poisoning and blurring of vision followed by field fedects with thallium poisoning. 4) Cerebellar disturbances: in the form of ataxia in organic mercury. 5) Parkinsonism: extrapyramidal signs occurs in manganese poisoning shown as mask face and rigidity of muscles. 6) Mental changes: as acute psychosis in organic lead and erethism in organic mercury.

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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.

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The present study deals with investigations on the general features of protein and iron metabolism under several conditions of chronic and acute liver damage induced by carbon tetrachloride. Data revealed a drop in the levels of serum total protein and albumin. The levels of alpha1, alpha2 and beta globulins were found to be increased. Gamma fraction was found to be proportionate with dosage accumulation and to varying extent. There were changes in haematocrit and haemoglobin values in all groups of chronic and acute carbon tetrachloride intoxicated rats. Also, there were no changes in reticulocyte count, plasma iron and total iron binding capacity levels in chronic intoxicated animals. However, in acute carbon tetrachloride plasma iron and total iron-binding capacity were significantly elevated.

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Investigations were performed to evaluate the activities of serum glutamic oxalacetic and glutamic pyruvic transaminases, alkaline phosphatase and lactate-dehydrogenase enzymes in rats intoxicated by different doses of carbon disulfide. Serum GOT and GPT activities were elevated which may be due to CS2 effect on cell membrane permeability. Serum-alkaline-phosphatase activity showed also increment, which was again attributed to the liver affection. A significant rise in serum-lactate-dehydrogenase activity which was referred to be as a result of muscle-lactate dehydrogenase release into the blood circulation.

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In alloxan diabetes, serum GOT, GPT, and ceruloplasmin were significantly increased compared to normal rats, while the level of serum alkaline phosphatale was decreased. Treatment with insulin led to lowering of serum GOT, GPT, and ceruloplasmin while serum alkaline phosphatase remained low. Then lycanol or daonil were used for treatment, serum GOT, GPT, and ceruloplasmin were changes towards normalization, while ceruloplasmin returned to normal values. Serum-alkaline phosphatase increased after 7 and 14 days from treatment with oral hypolygylcaemic drugs. In dithizonized diabetic animals, the levels of serum GOT, GPT, and alkaline phosphatase were found to be higher than normal, while ceruloplasmin levels were unchanged. After treatment with insulin all serum enzyme activities were normalized.

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The effect of carbon-tetrachloride poisoning and the protection caused by AMP were studied. A single dose of CCl4 has resulted in a rapid development of a fatty liver, a considerable increase in serum enzymes, glutamic oxalacetic and pyruvic transaminases as well as serum-alkaline phosphatase. Total serum protein showed a tendency to decrease accompanied by a decrease in A/G ratio. Administration of adenosine-5-monophosphate prevented the increase in serum-alkaline phosphatase and increased the A/G ratio. There was, however, a slight but significant decrease in serum GOT and GPT within the 24-hrs. period of study, but it remained still higher than that of the control. AMP lowered liver fat without complete protection against the development of fatty liver.

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Under the effect of carbon-disulfide intoxication on serum levels of zinc, iron, calcium, magnesium, potassium, and sodium of albino rats, five groups of rats were injected with daily doses of carbon disulfide over a period of 50 days. The extent of regression of the developed biochemical derangement was also studied. A significant decrease was observed in the levels of serum zinc, iron, calcium, and magnesium, while a slight elevation in the level of serum potassium. No definite correlation could be found between the level of serum sodium in control and carbon-disulfide intoxicated rats. By stoppage of dosage at 20 days, most of these derangements started to be normal.

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Under the effect of carbon-disulphide intoxication on the experimental animals, a significant decrease in serum copper and ceruloplasmin levels was observed. The decrease was aggravated with prolongation of carbon disulphide intoxication due to loss of appetite, formation of chelating compounds with carbon disulphide metabolites and increased loss of copper in urine. However, reinvestigated at 20 days after stoppage of dosage, most of these derangements started to be alleviated.

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In alloxan diabetes, serum zinc, copper, iron and magnesium were significantly higher than in normal rats, while the level of serum calcium, sodium, and potassium was lower than normal. Treatment with daonil or insulin led to a normalization, as expected of the level of serum glucose and most of the other elements, except for iron and potassium. When lycanol was used for treatment, the level of all elements returned to the normal except for blood glucose, zinc and potassium.

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