Beta vulgaris L. var cicla decreases liver injury induced by antiarrhytmic agent, Amiodarone.

Amiodarone (AMD) is an effective antiarrhythmic drug, but its long-term usage strongly forms liver toxicity due to its accumulation tendency. The chard is a unique plant which has a blood sugar-lowering effect and powerful antioxidant activity. The aim of the current study was to investigate the possible protective effects of chard on AMD-induced liver injury. Male Sprague-Dawley rats were divided into four groups. Control group, aqueous chard extract given group (500 mg/kg) day for one week, AMD given group (100 mg/kg) /day for one week, AMD+Chard given group (at the same doses and times). They were sacrificed on the 8th day. The blood and liver samples were taken. The serum and liver biochemical parameters were found to be changed in AMD treated group. Chard administration reversed these parameters in serum and liver. In histological experiments, necrotic areas, mononuclear cell infiltration, the endothelial rupture in central vein, sinusoidal dilatation, hyperemia, dark eosinophilic cells and picnotic nucleus were observed in liver tissues of AMD treated group. Chard treatment reduced liver tissue damage. Considering results, we can suggest that chard prevented AMD induced liver injury biochemically and histologically.

The effect of different types of microplastic and acute cadmium exposure on the Mytilus galloprovincialis (Lamarck, 1819).

Microplastic (MP) pollution is a pressing issue for both environmental health and the safety of human food sources. This study provides a comprehensive analysis of the effects of MPs on Mediterranean mussels (Mytilus galloprovincialis, Lamarck 1819), focusing on the food safety risks associated with MP and cadmium (Cd) exposure in these organisms intended for consumption. The retention of different polymer types of MPs in mussels was specifically evaluated, and the influence of Cd on MP retention across these polymers was investigated. Mussels were exposed to polystyrene (PS), polypropylene (PP), and polyethylene terephthalate (PET) MPs individually and in combination with the toxic metal Cd for a duration of 7 days. Antioxidant enzymes, oxidative stress parameters, and digestive system enzyme activities, selected as biomarkers for Cd and MPs pollution, were assessed. Furthermore, human consumption risk evaluations and limits regarding mussel intake were analysed in terms of food safety. The results suggest that exposure to Cd, MPs, or their combination induces oxidative stress, tissue damage, and neurotoxicity. Alterations in digestive enzyme activities could impact the mussels' energy acquisition from food and their capacity to conserve energy reserves. The estimated daily intake (EDI), provisional tolerable weekly intake (PTWI), target hazard quotient (THQ), and target cancer risk (TCR) levels for all groups surpassed established limits, implying a significant health risk for humans consuming these products. These results underscore the potential health risks for humans associated with consuming mussels exposed to Cd and/or MPs and provide valuable data for monitoring pollution levels and ecological risks in aquatic organisms. Additionally, our findings reveal that the retention of Cd in mussel tissues varies significantly after exposure, with combinations of PET and Cd showing lower levels of Cd accumulation compared to other groups, suggesting a differential interaction that influences Cd retention.

Reversal of Valproate-Induced Major Salivary Gland Changes By Moringa Oleifera Extract in Rats.

This study aimed to explore the potential protective impacts of Moringa oleifera extract on major alteration in salivary glands of rats exposed to sodium valproate (VA). Groups were defined as control, control+moringa extract, sodium valproate, and sodium valproate+moringa extract. Antioxidant and oxidant status, activities of digestive and metabolic enzymes were examined. VA treatment led to various biochemical changes in the salivary glands, including decreased levels of antioxidants like glutathione, glutathione-S-transferase, and superoxide dismutase (except for sublingual superoxide dismutase). Conversely, a decrease in alpha-amylase, alkaline and acid phosphatase, lactate dehydrogenase, protease, and maltase activities were observed. The study also demonstrated that VA induces oxidative stress, increases lipid peroxidation, sialic acid, and nitric oxide levels in the salivary glands. Total oxidant capacity was raised in all glands except in the sublingual gland. The electrophoretic patterns of proteins were similar. Moringa oleifera extract exhibited protective properties, reversing these VA-induced biochemical changes due to its antioxidant and therapeutic attributes. This research suggests that moringa extract might serve as an alternative treatment approach for individuals using VA and experiencing salivary gland issues, although further research is necessary to confirm these findings in human subjects.

Drug repurposing: Metformin's effect against liver tissue damage in diabetes and prostate cancer model.

Background: There are evidences linking diabetes to the pathogenesis and progression of various cancers. Metformin is a well-known antidiabetic drug that reduces the levels of circulating glucose and insulin in patients with both insulin resistance and hyperinsulinemia. Aim of the present study was to evaluate the effect of metformin on the liver of rats bearing prostate cancer, diabetes and prostate cancer + diabetes via histopathological and biochemical methods. Methods: Male Copenhagen rats were divided into six groups. Control group, diabetic group, cancer group, diabetic + cancer group, diabetic + cancer + metformin group, cancer + metformin group. Diabetes was induced by injecting single dose of streptozotocin (65 mg/kg) to Copenhagen rats, cancer induced 2 × 104 Mat-LyLu cells. Metformin treatment was administered daily by gavage following inocculation of the Mat- Lylu cells to fifth and sixth group. The experiment was terminated on the 14th day following Mat-LyLu cell injection. At the end of the experimental period, the rats were sacrificed, and liver tissue was taken. Liver damage was scored. Biochemically, serum prostate-specific antigen level was determined by employing Enzyme Linked Immuno Sorbent Assay method. In addition, the activities of different enzyme and biochemical parameters were determined spectrophotometrically inform the hepatic tissue specimens. Results: The findings of this study reveal that histopathological and biochemical damage in cancer and diabetic + cancer groups decreased significantly in the metformin treated groups. Conclusion: These highlights that the antidiabetic drug metformin can be repositioned for attenuating liver tissue damage associated with prostate cancer and diabetes.

Oxidative Brain Injury Induced by Amiodarone in Rats: Protective Effect of S-methyl Methionine Sulfonium Chloride.

Amiodarone (AMD) is a powerful antiarrhythmic drug preferred for treatments of tachycardias. Brain can be affected negatively when some drugs are used, including antiarrhythmics. S-methyl methionine sulfonium chloride (MMSC) is a well-known sulfur containing substance and a novel powerful antioxidant. It was intended to investigate the protective effects of MMSC on amiodarone induced brain damage. Rats were divided to four groups as follows, control (given corn oil), MMSC (50 mg/kg per day), AMD (100 mg/kg per day), AMD (100 mg/kg per day) + MMSC (50 mg/kg per day). The brain glutathione and total antioxidant levels, catalase, superoxide dismutase, glutathione peroxidase, paraoxonase, and Na+/K+-ATPase activities were decreased, lipid peroxidation and protein carbonyl, total oxidant status, oxidative stress index and reactive oxygen species levels, myeloperoxidase, acetylcholine esterase and lactate dehydrogenase activities were increased after AMD treatment. Administration of MMSC reversed these results. We can conclude that MMSC ameliorated AMD induced brain injury probably due to its antioxidant and cell protective effect.

The protective effect of vitamin U on pentylenetetrazole-induced brain damage in rats.

Pentylenetetrazole (PTZ) is preferred for experimental epilepsy induction. PTZ damages brain and other organs by elevating oxidative substances. Vitamin U (Vit U) is sulfur derivative substance that proved to be an excellent antioxidant. The current study was intended to determine the protective role of Vit U on PTZ-induced brain damage. Male Sprague-Dawley rats were separated into four groups. The Control group (Group I), was given saline for 7 days intraperitoneally (i.p); Vit U (Group II) was given as 50 mg/kg/day for 7 days by gavage; PTZ was injected into animals (Group III) at a single dose of 60 mg/kg, by i.p; PTZ + Vit U group (Group IV) was administered PTZ and Vit U in same dose and time as aforementioned. After the experiment was terminated, brain tissues were taken for the preparation of homogenates. In the PTZ group, glutathione and lipid peroxidation levels, alkaline phosphatase, myeloperoxidase, xanthine oxidase, acetylcholine esterase, antioxidant enzyme activities, total oxidant status, oxidative stress index, reactive oxygen species, and nitric oxide levels were increased. However, total antioxidant capacity was decreased in the PTZ group. Vit U ameliorated these effects in the PTZ-induced brain damage. Consequently, we can suggest that Vit U protected brain tissue via its antioxidant feature against PTZ kindling epilepsy.

Oxidative brain and cerebellum injury induced by d-galactosamine: Protective effect of S-methyl methionine sulfonium chloride.

The objective of this study was to examine the protective effects of S-methyl methionine sulfonium chloride (MMSC) against galactosamine (GalN)-induced brain and cerebellum injury in rats. A total of 22 female Sprague-Dawley rats were randomly divided into four groups as follows: Group I (n = 5), intact animals; Group II (n = 6), animals received 50 mg/kg/day of MMSC by gavage technique for 3 consecutive days; Group III (n = 5), animals injected with a single dose of 500 mg/kg of GalN intraperitoneally (ip); and Group IV (n = 6), animals injected with the same dose of GalN 1 h after MMSC treatment. After 6 h of the last GalN treatment (at the end of the experiments), all animals were killed under anesthesia, brain and cerebellum tissues were dissected out. Reduced glutathione, total antioxidant status levels, and antioxidant enzymes (catalase, superoxide dismutase, and glutathione-related enzymes), aryl esterase, and carbonic anhydrase activities remarkably declined whereas advanced oxidized protein products, reactive oxygen species, total oxidant status, oxidative stress index levels, and myeloperoxidase, acetylcholinesterase, lactate dehydrogenase, and xanthine oxidase activities were significantly elevated in the GalN group compared with intact rats. In contrast, the administration of MMSC to GalN groups reversed these alterations. In conclusion, we may suggest that MMSC has protective effects against GalN-induced brain and cerebellar toxicity in rats.

Gastroprotective effect of vitamin U in D-galactosamine-induced hepatotoxicity.

Galactosamine (GalN) is a well-known agent for inducing viral hepatitis models in rodents, but it can cause toxicity on different organs. Vitamin U (Vit U) has been proved as a powerful antioxidant on many toxicity models. The present study was designed to investigate the protective effects of Vit U on GalN-induced stomach injury. Rats were divided into four groups as follows: control (group I), Vit U given animals (50 mg/kg per day; group II), GalN administered animals (500 mg/kg at a single dose; group III), GalN + Vit U given animals (at the same dose and time, group IV). At the end of the 3rd day, animals were killed, and stomach tissues were taken. They were homogenized and centrifuged. In comparison to the control group, glutathione, total antioxidant capacity levels, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and Na+ /K+ -ATPase activities of GalN group were found to be decreased. On the contrary, lipid peroxidation, advanced oxidized protein products, hexose-hexosamine, fucose, sialic acid, reactive oxygen species levels, as well as the activities of myeloperoxidase, xanthine oxidase, and lactate dehydrogenase were elevated. Administration of Vit U reversed these abnormalities in the GalN group. It can be concluded that Vit U exerts its unique antioxidant effect and prevents GalN-induced gastric damage.

Lupeol inhibits pesticides induced hepatotoxicity via reducing oxidative stress and inflammatory markers in rats.

The present study was aimed at investigating the toxicity of various pesticides on rat liver. It also aimed to show whether this toxicity could be avoided using lupeol. Adult male Wistars albino rats were randomly divided into nine groups. Control groups were given saline, corn oil, and lupeol; pesticide groups were given malathion, chlorpyrifos, and tebuconazole; in the other three treatments, same doses of pesticides and lupeol were given to the rats for ten days. Histopathological examination showed severe degenerative changes in the pesticide groups. Serum AChE activities, liver GSH, total antioxidant capacity levels, AChE, CAT, SOD, GPx, GR, Na+/K+-ATPase, ARE, and PON were decreased, while serum TNF-α, liver LPO, HP, NO, AOPP, total oxidant status, ROS, and oxidative stress index levels as well as AST, ALT, ALP, GST, arginase and xanthine oxidase activities were increased in the pesticides administered groups. It was observed that the PCNA levels determined by the immunohistochemical method increased in the pesticide groups. Also, the results Raman spectroscopy suggest that the technique may be used to understand/have an insight into pesticide toxicity mechanisms. The administration of lupeol demonstrated a hepatoprotective effect against pesticide-induced toxicity.

The protective effect of metformin against testicular damage in diabetes and prostate cancer model.

Individuals with diabetes have an increased risk of breast, colorectal, pancreatic and prostate cancer. Metformin, an oral biguanide used to treat diabetes, has anti-hyperglycaemic, anti-hyperinsulinemic and antioxidant activities. The effects of metformin on testicular tissue damage in cancer and diabetic + cancer rat models were evaluated histologically, immunohistochemically and biochemically. The diabetic model was produced in Copenhagen rats using a single dose of streptozotocin (65 mg/kg), while prostate cancer was induced through subcutaneous inoculation of 2 × 104 Mat-LyLu cells into the animals. At the end of the experimental period, testicular tissues with a close functional relationship to the prostate were collected. Histological evaluation found moderate to severe damage to testes following the diabetes and cancer process. Histopathological and biochemical impairments were observed in the early stage of prostate cancer, which were increased in the diabetic animals. Metformin administration reversed these injuries and provided substantial protection of the testes. In particular, metformin had protective effects on tissue damage, apoptosis, oxidative stress and antioxidant capacity. This suggests that metformin should be further investigated as a targeted protective drug against prostate cancer-related damage to the testes.

Effect of vitamin B6 on brain damage in valproic acid induced toxicity.

Valproic acid (VPA) is an efficient antiepileptic drug widely used for the treatment of epilepsy and other seizures in both children and adults. It is also reported to have side and toxic effects on many organs and tissues. Vitamin B6 (Vit B6 ) is a well-described water-soluble vitamin, which has an antioxidant effect. In this study, we aimed to investigate the protective effect of Vit B6 on VPA-induced brain injury. Male Sprague-Dawley rats were divided into four groups. Group I, control animals; Group II, Vit B6 (50 mg/kg/day) given rats; Group III, VPA (500 mg/kg/day) given rats; Group IV, VPA and Vit B6 given rats at same dose and time. VPA and Vit B6 were administered intraperitoneally and orally, respectively, for 7 days. At the end of the experiments, the rats were sacrificed and brain tissues were taken. Protein carbonyl and sialic acid levels, xanthine oxidase, adenosine deaminase, acetylcholine esterase, lactate dehydrogenase, myeloperoxidase activities, total oxidant status, and reactive oxygen species levels were found to be increased, while glutathione and total antioxidant capacity levels, catalase, superoxide dismutase, glutathione-S-transferase, paraoxonase, and glutathione reductase activities were found to be decreased in the VPA group. Administration of Vit B6 reversed these defects in the VPA group. These findings indicate that Vit B6 has a protective effect on VPA-induced brain damage.

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.

Alpha-lipoic acid prevents brain injury in rats administered with valproic acid.

Valproic acid (VPA) is an effective drug, which is preferred for the treatments of epilepsy and various kinds of seizures. Nonetheless, VPA has many life-threatening side effects associated with free radical production. Alpha-lipoic acid (ALA) is a powerful antioxidant, which can scavenge reactive oxygen species (ROS). The effects of ALA against VPA-stimulated brain injury were investigated. In this study, Sprague-Dawley rats were divided as four groups: Group I, control rats; Group II, ALA-administered rats (50 mg/kg/d); Group III, VPA-administered rats (0.5 g/kg/d); Group IV: VPA- and ALA-administered rats at the same dose and time. According to the results, VPA increased lipid peroxidation, protein carbonyl, advanced oxidation protein products, total oxidant status, nitric oxide levels and glutathione-S-transferase, adenosine deaminase, xanthine oxidase activities, decreased glutathione, total antioxidant capacity levels, catalase, superoxide dismutase, glutathione peroxidase, sodium-potassium ATPase, and paraoxonase activities. Treatment with ALA reversed these effects. In conclusion, we may suggest that ALA may be a good candidate for prevention of VPA-induced brain injury.

The effects of vitamins and selenium mixture or ranitidine against small intestinal injury induced by indomethacin in adult rats.

This study was aimed at investigating morphological and biochemical efficacies of antioxidants on indomethacin-induced small intestinal damage in rats. Group I: control animals (negative control) given only placebo, Group II: (positive control) are animals orally given combination of antioxidants [vitamin C (Vit C), vitamin E (Vit E), ß-carotene and sodium selenite (Se)] daily for 3 days, Group III: Rats were given only indomethacin, Group IV: animals were given of antioxidants combination for 3 days, last dose was given 2 hr before the administration of indomethacin. Group V: Animals receiving ranitidine for 3 days (second positive control). Group VI: Animals received ranitidine for 3 days, last dose was given 2 hr before to indomethacin administration. Indomethacin caused degenerative morphological and biochemical changes, which were reversed on antioxidants administration. As a result, we propose that antioxidants combination would be therapeutically beneficial for treating indomethacin-induced lesions of small intestine. PRACTICAL APPLICATIONS: Indomethacin is a widely preferred nonsteroidal anti-inflammatory drug (NSAID) but its side effects on gastrointestinal system are well known. Indomethacin also causes production of reactive oxygen species. Antioxidants and selenium has protective effects. According to the results of this study, antioxidants and selenium can be used as a food supplement for preventing NSAID-induced side effects and toxicity.

The effects of antioxidant combination on indomethacin-induced gastric mucosal injury in rats.

The aim of this study is an investigation the protective effects of vitamin C (Vit C), vitamin E (Vit E), ß-carotene, sodium selenate combination in indomethacin-induced gastric mucosal damage in rats. Rats were divided into 6 groups. Group I: Intact animals (control). Group II: Control animals receiving Vit C (100 mg/kg/day), Vit E (100 mg/kg/day), ß-carotene (15 mg/kg/day) and sodium selenate (0.2 mg/kg/day) for 3 days. Group III: Animals receiving 25 mg/kg indomethacin. Group IV: Animals receiving Vit C, Vit E, ß-carotene and sodium selenate (in same doses) for 3 days 2 h before the administration of indomethacin. Group V: Animals receiving ranitidine (150 mg/kg) for 3 days. Group VI: Animals receiving ranitidine for 3 days 2 h before to the administration of indomethacin (in same dose and time). The administration of indomethacin caused a decrease in the levels of glutathione, mucus, hexosamine and in the activities of glutathione-S-transferase, sodium-potassium ATPase, thromboplastic activity and an increase in the aspartate and alanine amino transferase, alkaline phosphatase, catalase, lactate dehydrogenase, myeloperoxidase activities and sialic acid, lipid peroxidation and protein carbonyl levels.  Stomach caspase-8 immun+ cell numbers showed a slight increase while caspase-9 immun+ cell numbers reduced in indomethacin given group compared to control animals. Our results findings suggest that the combination of Vit C, Vit E, ß-carotene, sodium selenate and ranitidine has a protective effect on indomethacin-induced gastric mucosal injury of rats.

The effect of vitamin U on the lung tissue of pentyleneterazole-induced seizures in rats.

The aim of this study is to investigate the therapeutic effects of vitamin U (Vit U) on lung tissue of pentyleneterazole (PTZ)-induced seizures in rats. Sprague Dawley male rats were randomly divided into four groups as follows: control (0.9% NaCl given, intraperitoneally); Vit U (50 mg/kg/day, for 7 days by gavage); PTZ; (60 mg/kg one dose, intraperitoneally); and PTZ + Vit U (in same dose and time). At the end of the experiment, lung tissues were taken and examined biochemically and cytologically. Lipid peroxidation (LPO), glutathione (GSH), sialic acid (SA), and nitric oxide (NO) levels, and superoxide dismutase (SOD) and catalase (CAT) activities were determined in lung homogenates. Imprinted lung samples were stained with May Grunwald-Giemsa stain and microscopically examined for the presence of collagen fibers, macrophage, leucocyte, and epithelial cells. PTZ administration significantly increased GSH level and CAT activity and significantly decreased SOD activity compared to the control group. Vit U administration significantly increased GSH level and CAT activity compared to the control group. GSH and NO levels significantly decreased in PTZ + Vit U group compared to the PTZ group. In cytologic analysis, increased collagen fibers, macrophages, leucocytes, and epithelial cells were observed in PTZ group compared to the control group, and Vit U administration decreased these cytological parameters compared to the PTZ group. The findings of this study support the possible protective role of using Vit U as an add-on therapy in order to prevent lung tissue injury which may occur during seizures in epilepsy.

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.

Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties.

The aim of present study was to investigate the effect of vitamin U (vit U, S-methylmethionine) on oxidative stress, inflammation, and fibrosis within the context of valproic acid (VPA)-induced renal damage. In this study, female Sprague Dawley rats were randomly divided into four groups: Group I consisted of intact animals, group II was given vit U (50 mg/kg/day, by gavage), group III was given VPA (500 mg/kg/day, intraperitonally), and group IV was given VPA + vit U. The animals were treated by vit U 1 h prior to treatment with VPA every day for 15 days. The following results were obtained in vit U + VPA-treated rats: (i) the protective effect of vit U on renal damage was shown by a significant decrease in histopathological changes and an increase in Na(+)/K(+)-ATPase activity; (ii) anti-oxidant property of vit U was demonstrated by a decrease in malondialdehyde levels and xanthine oxidase activity and an increase in glutathione levels, catalase and superoxide dismutase activities; (iii) anti-inflammatory property of vit U was demonstrated by a decrease in tumor necrosis factor-α, interleukin-1ß, monocyte chemoattractant protein-1 levels, and adenosine deaminase activity; (iv) anti-fibrotic effect of vit U was shown by a decrease in transforming growth factor-ß, collagen-1 levels, and arginase activity. Collectively, these data show that VPA is a promoter of inflammation, oxidative stress, and fibrosis which resulted in renal damage. Vit U can be proposed as a potential candidate for preventing renal damage which arose during the therapeutic usage of VPA.