The aim of this study was to determine the effects of vitamin E deficiency on bone metabolism in growing female rats. The effects of supplementation of these vitamin E deficient rats with palm vitamin E, calcium or vitamin D3, alone or in combination on bone growth and metabolism were also studied. The rats were fed with vitamin E deficient diet and divided into 6 groups: unsupplemented (control, VED), VED + palm vitamin E 60 mg/kg rat weight (PVE60), VED + 1% calcium in drinking water, ad libitum (Ca), VED + vitamin D3, 0.5 g/kg rat weight (D), VED + PVE60/Ca, VED + PVE60/D. Calcium supplementation increased bone mineral density and reduced bone resorption activity in vitamin E deficient rats. Supplementation with palm vitamin E 60 mg/kg body weight/day, which is a mixture of 30% -tocopherols and 70% tocotrienols, increased bone calcium content, but failed to increase bone mineral density. Vitamin D3, (cholecalciferol) 0.5 g/kg did not increase bone mineral density or bone calcium content in vitamin E deficient rats. Combination of palm vitamin E and calcium or palm vitamin E and vitamin D3, in the same doses did not offer any added advantage to using each supplement alone. In conclusion, both calcium and vitamin E were needed for normal bone growth and development. Supplementation of vitamin D3, in a state of vitamin E deficiency was ineffective. However, the mechanism by which vitamin E deficiency impaired bone metabolism required further study.

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Dietary fat has been shown to enhance pancreatic carcinogenesis, but little is known of the effect of individual fatty acids. Administration of diet with altered fatty acid contents appears to effect the composition of rat pancreatic acinar cells. If administration of fatty acids can indeed alter the tissue fatty acid composition of pancreas, and can effect the development of preneoplastic foci, then it is possible that this may reflect in the target cells. In this study, in order to examine the particular effects of unsaturated (oleic) and saturated (stearic) fatty acids in development of pancreatic carcinogenesis, the fatty acid profiles of pancreatic tissues have been analyzed at a single time period (12 months). The findings of this study showed that in azaserine initiated oleic acid fed rats (AzOl Group) oleic acid caused an enrichment of tissue oleic acid content which was accompanied by a decrease in polyunsaturated linoleic, arachidonic and saturated stearic fatty acid levels. The results of this study may suggest that oleic acid can block the desaturation/elongation reactions leading from linoleic to arachidonic acid that polyunsaturated fatty acids may promote pancreatic carcinogenesis in this manner. The possibility remains that oleic acid may enhance tumorigenesis by a mechanism independent of prostaglandin production.

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The present investigation was undertaken to study short and long term effects of aluminium on acetylcholinestrase activity of different areas of rat brain.
Intraperitoneal administration of 2 mg/kg aluminium as AlCl3 daily for 15 to 60 days reduced acetylcholinestrase activity of cerebellum controls from 16.3 ± 0.7 to 14.2 ± 0.9, mid-brain from 15.8 ± 0.7 to 12.3 ± 0.7 and brain cortex from 8.7 ± 0.7 to 1.0 ± 0.4 mole enzyme/mg protein/min respectively (p < 0.05). Aluminium (10 mg/kg) administration daily for 15 and 30 days reduced acetylcholinestrase activity of cerebellum controls from 16.2 ± 0.8 to 12.1 ± 1.0, mid-brain from 15.8 ± 0.4 to 9.6 ± 0.5 and brain cortex from 8.4 ± 0.6 to 5.4 ± 0.4 mole enzyme/mg protein/min respectively (p < 0.05). Serum aluminium of aluminium treated animals was elevated significantly (p < 0.05). The neurotoxicity of aluminium has been considered in the discussion.

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In diabetic patients, the persistence of hyperglycemia has been reported as a cause of increased production of oxygen-free radicals through glucose autoxidation and nonenzymatic glycation. The antioxidant capacity is always decreased in diabetic patients, but it seems necessary to measure all the components to ascertain the reasons. The aim of this study was to determine the plasma total antioxidant capacity (TAC) and changes in the activities of two antioxidant enzymes; superoxide dismutase (SOD) and glutathion peroxidase (GPX) in diabetic patients and to estimate their relationship to levels of glycated hemoglobin, fasting blood sugar and duration of diabetes.
The changes in the status of antioxidant enzymes were evaluated in erythrocyte samples obtained from 125 diabetic patients (types I and II) and 120 apparently healthy sex and age matched subjects as control group. The activities of SOD and GPX were determined by standard spectrophotometric methods. Total antioxidant status was measured using Randox kit. Level of fasting blood glucose was measured by enzymatic method and that of glycated hemoglobin (GHb), by colorimetric method employing thiobarbituric acid reaction.
Serum glucose and GHb levels were high in two types of diabetic patients versus the control group. Compared with the control, the total antioxidant capacity was depleted in two diabetic groups, but depletion was more severe in second type. The activities of SOD and GPX were significantly low in two types of diabetic patients. Marked differences in the activities of the enzymes in good, fair and poor controlled patients were noticed. The enzyme activities in first type were higher than that of type II, but the differences were not significant. In diabetic patients, significant correlation between the total antioxidant capacity and levels of GHb, fasting blood sugar and duration of diabetes was observed, but in the case of SOD and GPX it was not marked.
In view of low activities of the enzymes in both types of diabetic patients and lack of correlation between their enzymes activities, levels of glycated hemoglobin, fasting blood sugar and duration of disease it may be concluded that reduction in the activities of the enzymes are partially involved in depletion of the total antioxidant capacity. It seems that the reduction in levels of other antioxidant enzymes and substances are involved in the decreased antioxidant capacity in diabetic patients. In view of low activities of SOD and GPX in patients supplementary trace elements such as Selenium, Copper, Zinc and Manganese, the essential components of the enzymes structures may be useful in prevention of oxidative stress. The meaningful correlation between depletion of total antioxidant capacity and poor glycemic control suggests that measurement of total antioxidant capacity in diabetic patients can be used as an index of glycemic control and development of diabetic complications in both types of diabetes.

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