18 research outputs found
ASSESSMENT OF THE POTENTIAL ROLE OF L- METHIONINE ON NICKEL SULFATE INDUCED RENAL INJURY AND OXIDATIVE STRESS IN RAT
No full textObjective: The study was designed to investigate the possible protective role of methionine (Met) in nickel sulfate induced oxidative stress in renal tissue.Methods: Rats were divided into the following groups: Healthy control; L-methionine (Met, 100 mg/kg, orally); nickel sulfate (Ni, 20 mg/kg, intraperitoneally); and combination Ni+Met. The experiment lasted 21 days. Antioxidant and renal function parameters with histological study were performed.Results: In the Ni group, marked renal damage was noticed with the significant elevation in the levels of creatinine, urea, and uric acid in serum. Animals also showed a significant rise in the lipid peroxidation level with a concomitant decrease in glutathione (GSH) and various antioxidant enzymes GSH peroxidase, catalase, and superoxide dismutase. Moreover, these changes in rats given the combined therapy nickel plus methionine were significantly less than those of group nickel, met prevented these alterations and maintained the antioxidant status. Histopathological examination of the kidney tissue proved the protective effect of Met against nickel toxicity.Conclusions: These results demonstrated that methionine augments antioxidant defense against nickel-induced toxicity and provides evidence that it has therapeutic potential as a renoprotective agent.</jats:p
CHARD (BETA VULGARIS VAR. CICLA) EXTRACT MODULATES ZINC STATUS, GLUCOSE LEVEL AND ANTIOXYDANT VALUES IN DIABETIC RATS FED ZINC DEFICIENCY DIET
No full textObjective: Oxidative stress which comes from hyperglycemia, it accelerates the development of cellular and vascular damage complications in diabetes, but the antioxidants may play a beneficial role in its prevention. Several plants extracts have an antioxidant activity and the ability to reduce oxidative stress in diabetes. Thus this study was conducted to investigate the effect of Beta vulgaris var cicla extract on zinc status, glucose concentration and antioxidant parameters in streptozotocin-diabetic rats fed zinc deficiency diet.Methods: Twenty-eight male albino (Wistar) rats were divided into four groups: two groups fed a zinc-sufficient diet one non-diabetic and the other diabetic, while the others two diabetic groups were fed a zinc-deficient diet, one non-treated group and the other treated with the extract of Beta vulgaris var cicla. After 21 d of dietary manipulation, fasting animals were scarified. Blood glucose, tissues zinc (femur, liver, kidney), malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) were evaluated.Results: Body weight gain of zinc-deficient diabetic animals was lower than that of zinc-adequate diabetic animals. It was noticed also that inadequate dietary zinc intake increased glucose and MDA levels. In addition, zinc deficiency diet led to a decrease in zinc tissues, GSH concentration both GST and GSH-Px activities. However, Oral administration of Beta vulgaris extract significantly decreased both serum glucose and MDA (p<0.001) levels, with a significant increase in body weight gain (p<0.001), GSH concentration (p<0.05, P<0.001), GST (p<0.05, p<0.001) and GSH-Px (p<0.001) activities.Conclusion: The present study showed that Beta vulgaris var cicla supplementation presumably acting as an antioxidant, and it can be a natural source for the reduction of diabetes development caused by zinc deficiency.</jats:p
THE BENEFIT EFFECT OF GINGER SUPPLEMENTATION AGAINST NICKEL-INDUCED HEPATOTOXICITY IN ALBINO WISTAR RATS
Get PDFObjective: This study was performed to study the potential capacity effect of ginger on the modulation effects of nickel-induced hepatotoxicity.
Methods: Thirty-two female albino Wistar rats were divided into four groups of eight each. One served as a control group, the second group (Gi) received ginger 20 g/kg diet, while the third group (Ni) was given nickel 800 mg/L in their drinking water as NiSO46H2O and the fourth group (Ni+Gi) was treated daily with both nickel and ginger. The experiment was lasted for 21 days.
Results: The exposure to nickel led to a significant decrease in body weight and food intake with an increase of liver weight. Nickel treatment also produced oxidative liver injury characterized by an increase of glucose, cholesterol, triglyceride, total lipids, bilirubin, malondialdehyde (MDA) concentrations and glutamate-pyruvate transaminase, glutamic oxaloacetic transaminase, and alkaline phosphatase activities. Meanwhile, serum total proteins and liver reduced glutathione (GSH) levels, catalase, GSH peroxidase, and GSH superoxide dismutase activities were decreased. These results are substantiated with marked changes in the histopathology, whereas the supplementation of ginger resulted in a restoration of the previous parameters.
Conclusion: It seems that ginger supplementation is a potent factor for reducing the oxidative severity of nickel hepatotoxicity through its antioxidant action
Effect of ginger on zinc, lipid profile and antioxidants levels in blood and liver of streptozotocin induced diabetic rats fed on zinc deficiency diet
Get PDF168-176Diabetes mellitus is a non-communicable disease affecting 463 million people across the world. Ginger has enormous health promoting potential effects in number of ailments including diabetes. So, the purpose of this study was to evaluate the beneficial effect of ginger (Zingiber officinale Roscoe) supplementation on carbohydrate metabolism, antioxidant status and tissue zinc in diabetic rats fed zinc deficient diet. Rats were divided into four groups. The first group was non-diabetic rats fed adequate zinc diet. The second was diabetic group fed also adequate zinc diet. While, the third and the fourth groups were diabetic fed zinc deficient diet, one non-treated and the other treated with ginger 2% diet. The findings showed an increase of blood glucose, transaminases, lipids profile and malondialdehyde levels, whereasinsulin, liverzinc, alkaline phosphatase, lactate dehydrogenase, proteins, reduced glutathione and antioxidant enzymes were reduced in zinc deficient rats. However, treatment with ginger restored the previous parameters. The obtained results indicated that ginger has a powerful effect, which led to a reduction of diabetes development in zinc deficiency due to its antioxidant potential
ASSESSMENT OF THE POTENTIAL ROLE OF L- METHIONINE ON NICKEL SULFATE INDUCED RENAL INJURY AND OXIDATIVE STRESS IN RAT
Get PDFObjective: The study was designed to investigate the possible protective role of methionine (Met) in nickel sulfate induced oxidative stress in renal tissue.Methods: Rats were divided into the following groups: Healthy control; L-methionine (Met, 100 mg/kg, orally); nickel sulfate (Ni, 20 mg/kg, intraperitoneally); and combination Ni+Met. The experiment lasted 21 days. Antioxidant and renal function parameters with histological study were performed.Results: In the Ni group, marked renal damage was noticed with the significant elevation in the levels of creatinine, urea, and uric acid in serum. Animals also showed a significant rise in the lipid peroxidation level with a concomitant decrease in glutathione (GSH) and various antioxidant enzymes GSH peroxidase, catalase, and superoxide dismutase. Moreover, these changes in rats given the combined therapy nickel plus methionine were significantly less than those of group nickel, met prevented these alterations and maintained the antioxidant status. Histopathological examination of the kidney tissue proved the protective effect of Met against nickel toxicity.Conclusions: These results demonstrated that methionine augments antioxidant defense against nickel-induced toxicity and provides evidence that it has therapeutic potential as a renoprotective agent
Combined protective effect of vitamins C and E on cadmium induced oxidative liver injury in rats
Get PDFOur study pertains to the potential ability of vitamin C and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress induced by cadmium. Male rats were randomly divided into five groups of eight each. Group I served as the controls; group II received in their drinking water CdCl2 (200 mg/L); group III received both CdCl2 and vitamin C (1.5 g/L of water); group IV was treated with CdCl2 and vitamin E (400 mg/kg diet); and group V received CdCl2 + vitamin C + vitamin E. The exposure of rats to cadmium chloride for 30 days resulted in a significant decrease in body weight gain. Cadmium treatment also produced oxidative liver injury characterized by increasing serum glucose concentration, glutamate-pyruvate transaminase (GPT), alanine aminotransaminase (GOT) and alkaline phosphatase (ALP) activities. Meanwhile cadmium supplementation decreased serum total protein and albumin in animals. In addition, liver glutathione level, catalase and glutathione peroxidase (GSH-Px) activities were diminished. With vitamin C and vitamin E administration during intoxication of cadmium, corrective effects on Cd-induced oxidative stress in the liver was observed. In conclusion, this study demonstrates that oral exposure to Cd caused reduction in LPO and antioxidant enzyme activities in rat’s liver, and vitamin C or vitamin E may have partial ameliorative effects on these disturbances, whereas vitamin C and vitamin E together assured a more efficient protection of the organ against the noticed oxidative stress.Key words: Cadmium, vitamin E, vitamin C, oxidative stress, glutathione, glutathione peroxidase, catalase
Preventive effect of zinc on nickel-induced oxidative liver injury in rats
Get PDFThis study pertains to the potential ability of zinc, used as nutritional supplements, to alternate oxidative stress induced by nickel. Male rats were randomly divided into four groups of eight each. Group I served as the controls; group II received in their drinking water ZnSO4 (227 mg/l); group III received NiSO4 (2 mg/100b.w/day intraperitoneally); group IV was treated with ZnSO4 and NiSO4. The exposure of rats to nickel sulfate for 21 days resulted in a significant decrease in body weight gain and absolute liver weight, relative liver weight. Nickel treatment also produced oxidative liver injury characterized by increasing serum glucose concentration, glutamate-pyruvate transaminase (GPT), alanine aminotransferase (GOT) and alkaline phosphatase (ALP) activities. Meanwhile nickel supplementation decreased serum total protein and albumin in animals. In addition, liver glutathione level, catalase and glutathione peroxidase (GSH-Px) activities were diminished. The administration of zinc with nickel (Ni + Zn) corrective effects on Ni-induced oxidative stress in liver was observed. In conclusion, this study demonstrates that intraperitoneally injection with Ni caused reduction in enzymes activities in rat’s liver and treatment with zinc offers a relative protection against nickel induced oxidative liver injury and lipid peroxidation probably due to its antioxidant proprieties.Key words: Nickel, zinc, rats, oxidative stress, liver
CHARD (BETA VULGARIS VAR. CICLA) EXTRACT MODULATES ZINC STATUS, GLUCOSE LEVEL AND ANTIOXYDANT VALUES IN DIABETIC RATS FED ZINC DEFICIENCY DIET
Get PDFObjective: Oxidative stress which comes from hyperglycemia, it accelerates the development of cellular and vascular damage complications in diabetes, but the antioxidants may play a beneficial role in its prevention. Several plants extracts have an antioxidant activity and the ability to reduce oxidative stress in diabetes. Thus this study was conducted to investigate the effect of Beta vulgaris var cicla extract on zinc status, glucose concentration and antioxidant parameters in streptozotocin-diabetic rats fed zinc deficiency diet.Methods: Twenty-eight male albino (Wistar) rats were divided into four groups: two groups fed a zinc-sufficient diet one non-diabetic and the other diabetic, while the others two diabetic groups were fed a zinc-deficient diet, one non-treated group and the other treated with the extract of Beta vulgaris var cicla. After 21 d of dietary manipulation, fasting animals were scarified. Blood glucose, tissues zinc (femur, liver, kidney), malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) were evaluated.Results: Body weight gain of zinc-deficient diabetic animals was lower than that of zinc-adequate diabetic animals. It was noticed also that inadequate dietary zinc intake increased glucose and MDA levels. In addition, zinc deficiency diet led to a decrease in zinc tissues, GSH concentration both GST and GSH-Px activities. However, Oral administration of Beta vulgaris extract significantly decreased both serum glucose and MDA (p<0.001) levels, with a significant increase in body weight gain (p<0.001), GSH concentration (p<0.05, P<0.001), GST (p<0.05, p<0.001) and GSH-Px (p<0.001) activities.Conclusion: The present study showed that Beta vulgaris var cicla supplementation presumably acting as an antioxidant, and it can be a natural source for the reduction of diabetes development caused by zinc deficiency
EFFECT OF SILYMARIN EXTRACTED FROM SILYBUM MARIANUM ON NICKEL HEMATOTOXICITY AND NEPHROTOXICITY IN MALE ALBINO WISTAR RATS
Get PDFObjective: The objective of this study was to investigate the effect of silymarin extract from Silybum marianum against nickel-induced alterations in haematological indices, kidney dysfunction and renal antioxidant defence system.Methods: Male albino Wistar rats were divided into four groups seven each. Control, silymarin, nickel and nickel plus silymarin. Silymarin was administrated orally (100 mg/kg b. wt) and nickel as nickel sulfate (NiSO4 6H20) was given intraperitoneally (20 mg/kg b. wt) at alternative days. The experiment continued for three consecutive weeks. Body weight was recorded regularly. After overnight fasting, animals were killed and serum creatinine, serum urea, serum uric acid, hematological parameters and renal antioxidant markers were determined.Results: The treatment with nickel led to a significant decrease in body weight with an increase in both absolute and relative kidney weights and a significant increase in renal markers, which confirmed by histopathological alteration. A microcytic anemia was also observed, which was manifested by a reduction of red blood cells count (RBC), hemoglobin (Hb) concentration, platelet counts (Plt), hematocrit and white blood cells counts (WBC). The level of lipid peroxidation was increased. Whereas, GSH concentration and enzymatic antioxidants SOD, GSH-Px and CAT activities were decreased. The co-treatment with methanolic extract of milk thistle attenuated the variation in the hematological and renal markers, decreasing renal lipid peroxidation (p<0.05) with a concomitant increasing reduced glutathione content (p<0.01) and restoring the antioxidant enzymes (SOD, CAT, GSH-Px) in kidney, as well as an improvement in histological changes compared to those previously noticed in nickel group.Conclusion: To conclude, these findings demonstrated that silymarin extract effectively improved heamatotoxicity and nephrotoxicity caused by nickel
The beneficial effect of combined administration of vitamins C and E on renal function and selected parameters of antioxidant system in diabetic rats fed zinc-deficient diet
Get PDFThe aim of this study was to examine the progression of kidney damage induced by zinc deficiency in diabetic rats and to evaluate the effect of combined treatment of vitamin E and vitamin C in renal injury by providing protection against deleterious action of zinc deficiency. Female diabetic albino Wistar rats were randomly assigned into five groups. The first group received a diet containing a 54 mg zinc/kg diet (adequate zinc, AZ), the second group received a diet containing 1 mg zinc/kg diet (zinc deficient group, ZD), and the three other groups received ZD diet and treated orally with vitamin E (500 mg/kg body wt) (ZD + Vit E), vitamin C (500 mg/kg body wt) (ZD + Vit C), and combined vitamins C and E (250 + 250 mg/kg body wt) (ZD+VitC+VitE), respectively. Body weight was recorded regularly (twice weekly). After four weeks of dietary manipulation, kidney zinc level, serum albumin and total protein concentration of ZD group were significantly lower than those of AZ group. Dietary zinc deficiency also increased proteinuria excretion, serum and urinary urea and uric acid levels, serum creatinine and kidney malondialdehyde concentration. In contrast, the catalase activity and reduced glutathione level in the kidney were reduced. In conclusion, vitamins E and C act as beneficial antioxidants protect renal function against the noticed oxidative stress due to zinc deficiency and experimental diabetes.Keywords: Experimental diabetes, zinc, vitamin E, vitamin C, oxidative stress, kidney damage
