جستجوی مقالات مرتبط با کلیدواژه « وانادیل سولفات » در نشریات گروه « پزشکی »

Diabetes mellitus is associated with changes in testicular tissue. Here, the effects of co-administration of zinc and vanadium sulfate on testicular damage in diabetic animals were studied.
Moderate diabetic hyperglycemia was induced by injection of streptozotocin (STZ) 40 mg/kg, ip. Five groups of animals were selected (n=5). Group I: As normal group, during the trial period did not receive any drug treatment and consumed tap water during 45 days. Group II: As control diabetic group, received STZ 40mg/kg, ip injection. During the trial period they did not receive any drug treatment and they consumed tap water. The diabetic animals (STZ 40mg/kg, ip) with 500-600 mg/dl blood glucose levels were randomly divided into three groups: Group III: As under treatment 1, used drinkable water containing 1mg/ml of vanadium sulfate Group IV: As under treatment 2, used drinkable water (0.25 mg/ml zinc sulfate) Group V: As under treatment 3, used drinkable water (1mg/ml of vanadium sulfate and 0.25 mg/ml zinc sulfate). Testicular damage were assessed using H & E staining.
Zinc sulfate and vanadium sulfate and their combination have reduced glucose plasma levels in diabetic rats. Vanadium sulfate reduced spermatogenesis and seminiferous tubule diameter in diabetic rats. Seminiferous tubule diameter and spermatogenesis have increased in diabetic rats receiving a combination of oral zinc and vanadium sulfate.
This study demonstrated that the use of zinc sulfate reduced testicular damage and can neutralize the negative effects of vanadium sulfate on testis in diabetic rats.

Vanadium (V) is a candidate to decrease the serum level of glucose in diabetic animal model. However, it affects the lipid peroxidation and antioxidant activity so could make nephrotoxicity and hepatotoxicity. In this study, the protective role of vitamin C as an antioxidant on nephrotoxicity and hepatotoxicity induced by vanadyl sulfate was investigated. This study was designed in 2 protocols. There were 3 groups in protocol 1 that received saline (group 1), saline daily for 7 days plus single dose of vanadyl sulfate (50 mg/kg intraperitoneally) in day 2 (group 2), or vitamin C (250 mg/kg intraperitoneally) daily for 7 days and single dose of vanadyl sulfate (group 3). There were 2 groups in protocol 2 that received saline plus single dose of vanadyl sulfate (50 mg/kg intraperitoneally) in day 2 (group 4) or vitamin C (250 mg/kg intraperitoneally) daily for 2 days plus single dose of vanadyl sulfate (group 5). At the end of experiment, blood samples were collected to measure serum level of blood urea nitrogen (BUN), creatinine (Cr), aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP), and all animals were sacrificed for histopathology investigation and determination of kidney tissue damage score (KTDS). In protocol 1, BUN/Cr ratio, kidney weight (KW), and KTDS decreased significantly in vanadyl sulfate plus vitamin C group in comparison with vanadyl sulfate plus saline group (P < 0.05). In addition, serum level of AST and ALP significantly decreased in vanadyl sulfate plus vitamin C group. In protocol 2, not only similar results were not observed, but also vitamin C increased the side effects of vanadyl sulfate. Administration of vitamin C as a potent antioxidant could decrease the vanadium-induced toxicity. So, as vanadyl sulfate can be used for diabetic model in laboratory, vitamin C can be useful to decrease the vanadium-induced nephrotoxicity and hepatotoxicity, too.

Considering insulin like effects of vanadium salts, these compounds have been evaluted as a therapeutic agent for treatment of diabetes mellitus in the experimental models of the disease in animals. This study was performed to study the ultrastructure of islet β cells in streptozotocin (STZ)- induced diabetes in rats after treatment with vanadyl sulfate (VS). Diabetes was induced in male Wistar rats by intravenous injection of 40 mg/kg STZ. Equal volume of normal saline was injected via lateral tail vein in sham animals. Seven days after injection animals in both groups were divided into treated and control groups.VS was added to the drinking water of the diabetic treated (DT) and Sham treated (NT) animals with a concentration of 0.5 mg/ml for one week and 1 mg/ml up to three months. Untreated diabetic (DC) and sham rats (NC) received tap water during this period. Two months later all animals were killed. Langerhans islets were isolated from exocrine parts by use of collagen digestion, and were fixed in glutaraldehyde. Ultrastructure of islet beta cells were studied by means of transmission electron microscope. VS treatment led to amelioration of the symptoms of diabetes including hyperglycemia and polydepsia in DT rats. DC rats remained diabetic during the period of study. No significant changes were observed in plasma glucose and fluid intake of NT animals. Ultrastructural studies of islet β cells of DT rats showed normal cells with normal chromatin distribution, well-developed rough endoplasmic reticulum, increased cytoplasmic granules and no clear sign of cell injury. Lymphocytic infiltration was not detected in langerhans islets of DT group. Nuclear pyknosis, cytoplasmic vacuolization, lymphocytic infiltration and signs of cell death such as cell necrosis were found in the islets of β cells of DC rats. Cytoplasm of islets β cells of NT rats were more granular in comparison to NC rats. Considering the results of this study we concluded that amelioration of diabetes signs in VS treated STZ induced diabetic rats are accompanied by preservation of islets β cell ultrastructure.