Effects of bovine enterovirus and type 1 diabetes on liver and kidney pyruvate kinase activity in an animal model

Type 1 diabetes (T1D) is an autoimmune disease characterized by the selective destruction of pancreatic beta cells. In addition to genetic factors, enteroviruses have been considered the main environmental factor involved in this pathology. Therefore, the objective of this study was to evaluate the effects of streptozotocin-induced diabetes and bovine enterovirus (BEV) on liver and kidney pyruvate kinase activity in rats. Fourteen male Wistar rats were divided in three groups: control, diabetes and a third group, which was fed with water experimentally contaminated by BEV. Increased blood glucose levels were found in both diabetes and enterovirus groups, whereas there were no alterations in the lipid profile. A reduced pyruvate kinase activity was observed in the liver and kidney of animals from diabetes and enterovirus groups. Under our experimental conditions, the ingestion of water experimentally contaminated by BEV induced alterations in glycaemia, and also interfered in the pyruvate kinase activity in liver and kidney of the rats, which might be one of the possible mechanisms involved in the T1D development.

Effects of bovine enterovirus and type 1 diabetes on liver and kidney pyruvate kinase activity in an animal model

Type 1 diabetes (T1D) is an autoimmune disease characterized by the selective destruction of pancreatic beta cells. In addition to genetic factors, enteroviruses have been considered the main environmental factor involved in this pathology. Therefore, the objective of this study was to evaluate the effects of streptozotocin-induced diabetes and bovine enterovirus (BEV) on liver and kidney pyruvate kinase activity in rats. Fourteen male Wistar rats were divided in three groups: control, diabetes and a third group, which was fed with water experimentally contaminated by BEV. Increased blood glucose levels were found in both diabetes and enterovirus groups, whereas there were no alterations in the lipid profile. A reduced pyruvate kinase activity was observed in the liver and kidney of animals from diabetes and enterovirus groups. Under our experimental conditions, the ingestion of water experimentally contaminated by BEV induced alterations in glycaemia, and also interfered in the pyruvate kinase activity in liver and kidney of the rats, which might be one of the possible mechanisms involved in the T1D development.(AU)

Effects of chronic exposure to hexavalent chromium in water on oxidative stress parameters in Wistar rats

Hexavalent chromium [Cr (VI)] is a metal utilized in different industries and consequently disposed in the environment. It is a toxic substance and its reduction to trivalent Cr [Cr (III)] generates intermediates, which are responsible for the oxidation of molecules, and cause the oxidative stress. Therefore, the aim of this study was to evaluate if Cr (VI) could induce oxidative stress in Wistar rats. In this study, Wistar rats were chronically exposed to 25 and 50 ppm of potassium dichromate in drinking water for 30 days. The levels of Cr were evaluated in the blood and tissues (liver, kidneys, and lungs). Oxidative stress was determined in the liver, kidneys, and lungs and was evaluated by DFCH, TBA-RS and carbonyl test. Antioxidant enzymes were evaluated through catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Regarding the results, Cr concentration was significantly elevated in all tissues, however, it was lower in the lungs. In relation to the oxidative stress parameters, there was a significant increase of DCFH levels in the kidneys and carbonyls in liver and kidneys. Regarding the antioxidant enzymes, SOD was decreased in all organs and GPx was diminished in the kidneys. These data indicated that Cr (VI) could induce oxidative stress in the kidneys and liver due to an imbalance between oxidative and antioxidant parameters. The lungs were little affected, possibly by the lowest chromium accumulation.

Effects of chronic exposure to hexavalent chromium in water on oxidative stress parameters in Wistar rats

Hexavalent chromium [Cr (VI)] is a metal utilized in different industries and consequently disposed in the environment. It is a toxic substance and its reduction to trivalent Cr [Cr (III)] generates intermediates, which are responsible for the oxidation of molecules, and cause the oxidative stress. Therefore, the aim of this study was to evaluate if Cr (VI) could induce oxidative stress in Wistar rats. In this study, Wistar rats were chronically exposed to 25 and 50 ppm of potassium dichromate in drinking water for 30 days. The levels of Cr were evaluated in the blood and tissues (liver, kidneys, and lungs). Oxidative stress was determined in the liver, kidneys, and lungs and was evaluated by DFCH, TBA-RS and carbonyl test. Antioxidant enzymes were evaluated through catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Regarding the results, Cr concentration was significantly elevated in all tissues, however, it was lower in the lungs. In relation to the oxidative stress parameters, there was a significant increase of DCFH levels in the kidneys and carbonyls in liver and kidneys. Regarding the antioxidant enzymes, SOD was decreased in all organs and GPx was diminished in the kidneys. These data indicated that Cr (VI) could induce oxidative stress in the kidneys and liver due to an imbalance between oxidative and antioxidant parameters. The lungs were little affected, possibly by the lowest chromium accumulation.(AU)