Form Of Zinc Sulphate Research Articles

Alcoholic myopathy: Lack of effect of zinc supplementation

A chronic form of myopathy has been described in alcoholics, characterized by atrophy of type II fibers, due both to reduced protein synthesis and increased protein breakdown. Increased production of reactive oxygen species could probably play a role in increased protein breakdown. In addition, treatment with zinc might be beneficial, since it acts as a cofactor of several enzymes involved in the synthesis of proteins and antioxidants as copper-zinc-superoxidedismutase (SOD) and selenium dependent glutathione peroxidase (GPX). Based on these facts, we analyze the relative and combined effects of ethanol, protein malnutrition and treatment with zinc, 227 mg/l in form of zinc sulphate, on muscle changes in 8 groups of adult Sprague–Dawley rats fed following the Lieber–de Carli model during 5 weeks. We also study the association between muscle histological changes and the activity of GPX, SOD and lipid peroxidation products (MDA), with hormones such as IGF-1, and with trace elements involved in antioxidant systems and/or in lipid peroxidation, such as selenium, copper, zinc, and iron. We found type IIa and IIb fiber atrophy in the alcoholic animals, especially in the low-protein fed ones. This effect was mainly due to protein deficiency. Zinc played no role at all. Muscle iron increased in ethanol, low protein fed rats, either with or without zinc, and was directly related with muscle MDA levels, which in turn were related with muscle atrophy, as was also found for serum IGF-1 levels. Ethanol was the main responsible for all these changes, although protein undernutrition also played an independent role in MDA levels. A positive interaction between ethanol and protein deficiency on serum IGF-1 was also detected. These results suggest that both protein deficiency and ethanol contribute to muscle atrophy observed in alcoholized rats; this atrophy is associated with increased lipid peroxidation and muscle iron overload. Treatment with zinc sulphate confers no benefit.

Infrared studies on the effect of zinc on black‐gram

Abstract An attempt was made to study the influence of zinc (Zn) on organic constituents like polysacharides, aminoacids, and chlorophyll using an infrared (IR) technique. Zinc was applied to a soil in the form of zinc sulphate (ZnSO4) in different concentrations in which the blackgram plants were grown. The plant leaves were sampled at 30, 45, and 65 days after sowing and analyzed by IR. Intensity variations were observed with age of the plant leaves and with applied Zn concentration. The extinction coefficient ‘k’ was calculated for the prominent absorption bands at 3380, 2928, 1651, and 1026/cm in the near IR. The variations of ‘k’ values with age and concentration of Zn appear to vary linearly with the variations of essential amino acid content in blackgram leaves. The values of ‘k’ increased with low concentrations of Zn upto 150 mg/kg, while higher concentrations decreased the ‘k’ values.

Renal metallothionein metabolism after a reduction of renal mass. II. Effect of zinc pretreatment on the renal toxicity and intrarenal accumulation of inorganic mercury

In the present study we examined the effects of zinc pretreatment (to induce the renal synthesis of metallothionein) on the renal accumulation and intrarenal distribution of inorganic mercury in uninephrectomized (NPX) and sham-operated (SO) rats 24 h after the animals were given a 0.75, 1.0 or 1.5 μmol/kg intravenous (i.v.) dose of inorganic mercury. We also examined the effects of zinc pretreatment on the nephropathy induced by the three doses of inorganic mercury. Zinc was administered at a dose of 306 μmol/kg (20 mg/kg) subcutaneously (s.c.) in the form of zinc sulfate once daily for 2 consecutive days prior to the administration of inorganic mercury. Following zinc pretreatment, the renal accumulation of injected inorganic mercury increased in both NPX and SO rats treated with the three doses of inorganic mercury, but the increase was significantly greater in the NPX rats. The enhanced accumulation of mercury was associated with an altered pattern in the intrarenal distribution of mercury, particularly in the NPX rats. The increased renal accumulation of mercury in both the NPX and SO rats was due primarily to its increase in the renal cortex. We have recently found that the synthesis of metallothionein in the renal cortex increases in NPX and SO rats given zinc. Therefore, it appears that there is a relationship between the content of preinduced cellular metallothioein in the cortex and the content of mercury that accumulates in the cortex. Zinc pretreatment also prevented the nephropathy induced by the three doses of inorganic mercury from occurring in both the NPX and SO rats. We propose that some of the protection may be related to the altered intrarenal accumulation and distribution of mercury that occurs after pretreatment with zinc. Hepatic accumulation of mercury also increased in both groups of rats, but increase again was significantly greater in the NPX rats. Our findings show clearly that a significant reduction in renal mass alters the hepatic and renal accumulation of mercury when zinc pretreatment is used to induce the renal and hepatic synthesis of metallothinein. In addition, our findings show that zinc pretreatment protects both normal and remnant kidneys in rats from the nephrotoxic effects of inorganic mercury.

High Zinc Supplementation of Rainbow Trout Diets

Abstract Zinc in the form of zinc sulfate or chelated as zinc proteinate was fed in increasing levels (4 to 1,700 µg/g zinc) in an egg-white based diet to fingerling rainbow trout (Salmo gairdneri) to determine potential toxicity. Zinc sulfate was fed for the first 55 days and zinc proteinate for the last 118 days of a 173-day test. Fish fed the lowest level of zinc (4 µg/g zinc, a zinc-deficient diet) had poor growth and high mortalities, while the lowest level of added zinc (90 µg/g) reduced mortalities and markedly improved growth. Higher levels of supplemented zinc, up to 1,700 µg/g, had no further effect on growth or survival. Zinc concentration in liver, blood, and gills increased with dietary levels of zinc above 90 µg/g. Trout showed no signs of zinc toxicity during feeding with levels of dietary zinc as high as 1,700 µg/g.