Protective role of zinc in liver damage in experimental diabetes demonstrated via different biochemical parameters.

Diabetes mellitus is a serious worldwide metabolic disease, which is accompanied by hyperglycaemia and affects all organs and body system. Zinc (Zn) is a basic cofactor for many enzymes, which also plays an important role in stabilising the structure of insulin. Liver is the most important target organ after pancreas in diabetic complications. In this study, we aimed to investigate the protective role of Zn in liver damage in streptozotocin (STZ)-induced diabetes mellitus. There are four experimental groups of female Swiss albino rats: group I: control; group II: control + ZnSO4 ; group III: STZ-induced diabetic animals and group IV: STZ-diabetic + ZnSO4 . To induce diabetes, STZ was injected intraperitoneally (65 mg/kg). ZnSO4 (100 mg/kg) was given daily to groups II and IV by gavage for 60 days. At the end of the experiment, rats were killed under anaesthesia and liver tissues were collected. In the diabetic group, hexose, hexosamine, fucose, sialic acid levels, arginase, adenosine deaminase, tissue factor activities and protein carbonyl levels increased, whereas catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase and Na+ /K+ -ATPase activities decreased. The administration of Zn to the diabetic group reversed all the negative effects/activities. According to these results, we can suggest that Zn has a protective role against STZ-induced diabetic liver damage.

Zinc Supplementation Restores Altered Biochemical Parameters in Stomach Tissue of STZ Diabetic Rats.

The stomach is among the organs grossly affected organ by diabetic complications. The present study was aimed at investigating the protective role of zinc on stomach of streptozotocin (STZ)-induced diabetes mellitus. Female Swiss albino rats were divided in four experimental groups: Group I, control; group II, control + zinc sulfate; group III, STZ-induced diabetic animals; and group IV, STZ-diabetic + zinc sulfate. Diabetes was induced by intraperitoneal injection of STZ, at a dose of 65 mg/kg body weight. Zinc sulfate (100 mg/kg body weight) was given daily by gavage for 60 days to groups II and IV. At the end of the experiment, the rats were sacrificed, and the tissues were taken. In the diabetic group, hexose, hexosamine, fucose, and sialic acid levels, as well as tissue factor, adenosine deaminase, carbonic anhydrase, xanthine oxidase, lactate dehydrogenase, prolidase activities, advanced oxidized protein products, homocysteine, and TNF-α levels were increased in the stomach tissue homogenates. Whereas, catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase, paraoxonase, and aryl esterase activities were decreased in the diabetic group. The administration of zinc reversed all the deformities. These findings suggest that zinc has protective role in ameliorating several mechanisms of STZ-induced diabetic stomach injury.

Zinc supplementation ameliorates glycoprotein components and oxidative stress changes in the lung of streptozotocin diabetic rats.

Zinc (Zn) is a component of numerous enzymes that function in a wide range of biological process, including growth, development, immunity and intermediary metabolism. Zn may play a role in chronic states such as cardiovascular disease and diabetes mellitus. Zn acts as cofactor and for many enzymes and proteins and has antioxidant, antiinflammatory and antiapoptotic effects. Taking into consideration that lung is a possible target organ for diabetic complications, the aim of this study was to investigate the protective role of zinc on the glycoprotein content and antioxidant enzyme activities of streptozotocin (STZ) induced diabetic rat tissues. Female Swiss albino rats were divided into four groups. Group I, control; Group II, control + zinc sulfate; Group III, STZ-diabetic; Group IV, diabetic + zinc sulfate. Diabetes was induced by intraperitoneal injection of STZ (65 mg/kg body weight). Zinc sulfate was given daily by gavage at a dose of 100 mg/kg body weight every day for 60 days to groups II and IV. At the last day of the experiment, rats were sacrificed, lung tissues were taken. Also, glycoprotein components, tissue factor (TF) activity, protein carbonyl (PC), advanced oxidative protein products (AOPP), hydroxyproline, and enzyme activities in lung tissues were determined. Glycoprotein components, TF activity, lipid peroxidation, non enzymatic glycation, PC, AOPP, hydroxyl proline, lactate dehydrogenase, catalase, superoxide dismutase, myeloperoxidase, xanthine oxidase, adenosine deaminase and prolidase significantly increased in lung tissues of diabetic rats. Also, glutathione levels, paraoxonase, arylesterase, carbonic anhydrase, and Na(+)/K(+)- ATPase activities were decreased. Administration of zinc significantly reversed these effects. Thus, the study indicates that zinc possesses a significantly beneficial effect on the glycoprotein components and oxidant/antioxidant enzyme activities.

Alterations in kidney tissue following zinc supplementation to STZ-induced diabetic rats.

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.

The influence of zinc supplementation on the pancreas of streptozotocin-diabetic rats.

The aim of this study was to investigate the effects of zinc supplementation on somatostatin and insulin peptide expressions and biochemical parameters. Six- to 6.5-month-old female Swiss albino rats weighing 150-200 g were used. The animals were divided into four groups: group I: control (intact) animals; group II: control animals given zinc sulfate; group III: streptozotocin (STZ)- induced diabetic animals; group IV: STZ-induced diabetic animals given zinc sulfate. Fasting blood glucose and glutathione levels were measured at 0, 1, 30 and 60 days. On day 60, the pancreas tissue and blood samples were taken from the animals. Zinc supplementation caused a decrease in hyperglycemia, as well as weight increase. Zinc sulfate treatment did not affect the number of somatostatin-immunoreactive cells in the pancreas. More insulin-immunoreactive cells were observed in the pancreatic islets of the diabetic+zinc sulfate group than in the diabetic group, although it was not statistically significant. The results show that zinc supplementation may prevent diabetes in experimental animals.

Effects of hyperbaric oxygen and Pgg-glucan on ischemic colon anastomosis.

AIM: In colorectal surgery, anastomotic failure is still a problem in ischemia. Here,we analyzed the effects of hyperbaric oxygen and beta-glucan on colon anastomoses in ischemic condition. METHODS: Colonic resection and anastomosis in rectosigmoid region were done in forty Wistar-Albino rats of four groups of equal number. Colon mesentery was ligated to induce ischemia. The first group was the control group. The subjects of second group were treated with hyperbaric oxygen;the third group with glucan and the forth group were treated with both. At the forth day, rats were sacrificed,anastomotic segment was resected and burst pressures and hydroxyproline levels of anastomotic line were measured. RESULTS: The burst pressure difference of second and third groups from the control group were meaningful (P<0.01); the forth group differed significantly from the control (P<0.001). There was no difference between the treated groups on burst pressure level (P>0.05). The hydroxyproline levels in all treated groups were different from the control group significantly (P<0.001). Hydroxyproline levels in the forth group were higher than those of the second and the third groups (P<0.001). There were no significant differences between the second and the fourth groups in burst pressure and hydroxyproline levels (P>0.05). CONCLUSION: Hyperbaric oxygen and glucan improve healing in ischemic colon anastomoses by anti-microbic,immune stimulating properties and seem to act synergistically when combined together.

Alterations in somatostatin cells and biochemical parameters following zinc supplementation in gastrointestinal tissue of streptozotocin-induced diabetic rats.

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.