Gene/Protein Disease Symptom Drug Enzyme Compound
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This study was designed to evaluate the protective effects of zinc on the liver activities of antioxidant enzymes in protein-deficient rats. Zinc sulfate at a dose level of 227 mg/l in drinking water was administrated to Sprague Dawley normal control as well as to protein-deficient rats for a total duration of eight weeks. The effects of zinc treatment and protein deficiency alone as well as combined were studied on rat liver antioxidant enzymes which included catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), and glutathione S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic lipid peroxidation and in catalase, Gpx, GR and GST activity. A significant inhibition in the levels of SOD activity and reduced glutathione (GSH) was observed following protein deficiency in normal rats. Zn treatment to protein deficient animals lowered lipid peroxidation and catalase, Gpx and GST activities, and also resulted in a significant elevation in the levels of GSH and SOD activity. The concentration of zinc decreased significantly in protein deficient animals but returned to normal levels when zinc was administered.
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PMID:Protective effects of zinc on oxidative stress enzymes in liver of protein deficient rats. 1567 49

Persons afflicted with protein malnutrition are generally deficient in a variety of essential micronutrients like zinc, copper, iron, and selenium, which in turn affects number of metabolic processes in the body. To evaluate the protective effects of zinc on the enzymes involved in oxidative stress induced in liver of protein-deficient rats, the current study was designed. Zinc sulfate at a dose level of 227 mg/L zinc in drinking water was administered to female Sprague-Dawley normal control as well as protein-deficient rats for a total duration of 8 weeks. The effects of zinc treatment in conditions of protein deficiency were studied on rat liver antioxidant enzymes, which included catalase, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), glutathione reduced (GSH), and glutathione-S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic activities of catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase and the levels of lipid peroxidation. A significant inhibition in the levels of reduced glutathione and the enzyme activity of superoxide dismutase has been observed after protein deficiency in normal rats. Interestingly, Zn treatment to protein-deficient animals lowered already raised activity catalase, glutathione peroxidase, and glutathione-S-transferase and levels of lipid peroxidation to significant levels when compared to protein-deficient animals. Also, Zn treatment to the protein-deficient animals resulted in a significant elevation in the levels of GSH and SOD activity as compared to their respective controls, thereby indicating its effectiveness in regulating their levels in adverse conditions. It has also been observed that concentrations of zinc, copper, iron, and selenium were found to be decreased significantly in protein-deficient animals. However, the levels of these elements came back to within normal limits when zinc was administrated to protein-deficient rats. This study concludes that zinc has the potential to regulate the activities of oxidative stress enzymes as well as essential hepatic elements.
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PMID:Protective effects of zinc on oxidative stress enzymes in liver of protein-deficient rats. 1586 62

Chronic hyperglycemia in diabetes is a major causative factor of free radical generation which further leads to many secondary diabetic complications via the damage to cellular proteins, membrane lipids, and nucleic acids. Zinc is an essential trace element in all living systems and plays a structural role in many proteins and enzymes. Somatostatin is known to have inhibitory effects on various gastrointestinal functions. Therefore, we determined somatostatin protein production and secretion levels, and biochemical and light microscopical changes following zinc supplementation in the gastrointestinal tract of streptozotocin (STZ)-diabetic rats. The animals were divided into four groups: Group I: control (untreated) animals; Group II: control animals given zinc sulfate; Group III: diabetic animals; and Group IV: diabetic animals given zinc sulfate. Zinc sulfate was given to the animals by gavage at a daily dose of 100 mg/kg body weight for 60 days. Diabetes was induced by intraperitoneal (i.p.) injection of STZ in a single dose of 65 mg/kg. For histological studies, stomach and duodenum tissues were fixed in Bouin solution and sections stained with Masson's trichrome and Periodic-Acid-Schiff. Tissue homogenates were used for protein, lipid peroxidation (LPO), glutathione (GSH), and nonenzymatic glycosylation (NEG) analyses. Zinc supplementation to the STZ-diabetic rats revealed the protective effect of zinc on these parameters. Zinc supplementation may contribute to prevent at least some complications of diabetes mellitus.
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PMID:Alterations in somatostatin cells and biochemical parameters following zinc supplementation in gastrointestinal tissue of streptozotocin-induced diabetic rats. 1746 Jul 67

Diabetes mellitus is a chronic disease characterized by anomalies forming in carbohydrate, lipid, protein metabolisms and the incidence of this disease varies widely throughout the world. Zinc is an important element which is essential for life and is present in nature. In this study, the animals were divided into four groups. These groups were named as untreated; zinc sulfate; streptozotocin (STZ); STZ and zinc sulfate. STZ (65 mg/kg) was dissolved in a freshly prepared 0.01 M pH 4.5 citrate buffer and given with intraperitoneal injection in a single dose. Zinc sulfate (100mg/kg) was dissolved in distilled water and given to the animals by gavage at a daily dose for 60 days. The rats were sacrificed under ether anesthesia. This study was aimed to investigate histological and biochemical changes of zinc supplementation on the kidney tissue in STZ-induced diabetic rats. In the current study, histological and histochemical observations showed that the occurred degenerative changes decreased after giving zinc in the kidney tissue of diabetic group. Kidney glutathione (GSH) levels decreased and lipid peroxidation (LPO), nonenzymatic glycosylation (NEG), urea and creatinine levels increased in diabetic rats. GSH levels increased, while LPO, NEG, urea and creatinine levels decreased in the kidney with administration of zinc to diabetic rats. As a result, we observed curative effects of zinc given to diabetic rats. We can say that zinc may be an important antioxidant for the treatment of secondary complications of diabetes in kidney tissue.
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PMID:Alterations in kidney tissue following zinc supplementation to STZ-induced diabetic rats. 2294 85

Soil salinity is the main obstacle to worldwide sustainable productivity and food security. Zinc sulfate (Zn) and paclobutrazol (PBZ) as a cost-effective agent, has multiple biochemical functions in plant productivity. Meanwhile, their synergistic effects on inducing salt tolerance are indecisive and not often reported. A pot experiment was done for evaluating the defensive function of Zn (100 mg/L) or PBZ (200 mg/L) on salt (0, 50, 100 mM NaCl) affected pea plant growth, photosynthetic pigment, ions, antioxidant capacity, and yield. Salinity stress significantly reduces all growth and yield attributes of pea plants relative to nonsalinized treatment. This reduction was accompanied by a decline in chlorophyll, nitrogen, phosphorus, and potassium (K+), the ratio between K+ and sodium (Na+), as well as reduced glutathione (GSH) and glutathione reductase (GR). Alternatively, salinity increased Na+, carotenoid (CAR), proline (PRO), ascorbic acid (AsA), superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) over nonsalinized treatment. Foliar spraying with Zn and PBZ under normal condition increased plant growth, nitrogen, phosphorus, potassium, K+/Na+ ratio, CAR, PRO, AsA, GSH, APX, GR, and yield and its quality, meanwhile decreased Na+ over nonsprayed plants. Application of Zn and PBZ counteracted the harmful effects of salinity on pea plants, by upregulating the antioxidant system, ion homeostasis, and improving chlorophyll biosynthesis that induced plant growth and yield components. In conclusion, Zn plus PBZ application at 30 and 45 days from sowing offset the injuries of salinity on pea plant growth and yield by upregulating the antioxidant capacity and increasing photosynthetic pigments.
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PMID:Zinc and Paclobutrazol Mediated Regulation of Growth, Upregulating Antioxidant Aptitude and Plant Productivity of Pea Plants under Salinity. 3293 48