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We investigated the protective effect of the NADPH oxidase inhibitor apocynin on testicular damage induced by ischemia-reperfusion injury in rats.A total of 32 rats were randomly divided into 4 groups. Controls underwent left scrotal exploration only. The 3 groups with ischemia-reperfusion underwent 4-hour torsion followed by 1-hour detorsion. The ischemia-reperfusion only group underwent left testicular torsion and detorsion. The ischemia-reperfusion plus saline group underwent left testicular torsion, received 10 ml/kg saline intraperitoneally at minute 210 of ischemia and then underwent detorsion. The ischemia-reperfusion plus apocynin group underwent left testicular torsion, received 20 mg/kg apocynin intraperitoneally at minute 210 of ischemia and then underwent detorsion. We determined histopathological findings and performed specific biochemical analyses.In the ischemia-reperfusion only and the ischemia-reperfusion plus saline groups malondialdehyde, total oxidative capacity and the oxidative stress index were significantly higher. Superoxide dismutase, catalase, glutathione peroxidase and glutathione were significantly lower. Apocynin significantly decreased malondialdehyde, total oxidative capacity and the oxidative stress index, and significantly increased superoxide dismutase and catalase. There was a significantly increase in the number of giant, degenerated and desquamated cells in the ischemia-reperfusion group. Apocynin significantly improved these histological alterations.These histopathological and biochemical findings show the beneficial effects of apocynin on testicular ischemia-reperfusion injury.

Dexmedetomidine (dex) is a potent, highly selective and specific α2-adrenoreceptor agonist. This experimental study was designed to investigate protective and therapeutic effect of two different doses of dex, on kidney damage induced by ischemia-reperfusion (I/R) in rats. Male Sprague-Dawley rats were divided into four groups, each including 10 animals: control group, ischemia-reperfusion (I/R) group; treated groups with 10 μg/kg of dex and 100 μg/kg of dex. After removing right kidney of the rats, the left kidney has performed ischemia during 40 min and reperfusion in the following 3 h. The histopathological findings, and also tissue superoxide dismutase (SOD) and catalase (CAT) enzyme activity, malondialdehyde (MDA), glutathione (GSH), serum blood urea nitrogen (BUN), creatinine (Cre) and tumor necrosis factor-alpha (TNF-α) levels were determined. In the I/R group, compared to the control group, levels of BUN, Cre and kidney tissue MDA have increased significantly, SOD, CAT enzyme activity and glutathione levels have decreased significantly. In the dex10 group, compared to the I/R group, levels of Cre and TNF-α have decreased significantly, while the SOD activity has increased significantly. In the dex100 group, compared to the I/R group, levels of BUN, Cre have decreased significantly, while the SOD activity has increased significantly. In the I/R group, there was also extensive tubular necrosis, glomerular damage in the histological evaluation. Dex ameliorated these histological damages in different amounts in two treatment groups. In this study, the protective effects of dex against renal I/R injury have been evaluated by two different amount of doses.

The aim of this study was to evaluate the acute effect of high-dose acetylsalicylic acid (ASA) on kidney and testis, and the potential protective and therapeutic effects of melatonin on ASA-related pathology. A total of 40 rats were randomly divided into the following 5 groups ( n = 8): group 1: control, not given any drug; group 2: only 200 mg/kg ASA was given; group 3: 5 mg/kg melatonin was given 45 min before administering 200 mg/kg ASA; group 4: 5 mg/kg melatonin was given 45 min after administering 200 mg/kg ASA; and group 5: only 5 mg/kg melatonin was given. The histopathological changes and the biochemical findings; such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), reduced glutathione (GSH), and blood urea nitrogen (BUN) as well as serum creatinine (Cr) levels were evaluated. ASA significantly increased MDA levels in both kidney and testis, whereas it significantly decreased the values of SOD, CAT, GPX, and GSH in kidney and CAT levels in testis. Melatonin significantly decreased MDA levels in kidney and ameliorated it in testis, whereas it caused elevation in the levels of antioxidants. BUN and Cr levels were higher after ASA, whereas these levels were diminished after melatonin administration. The improvement obtained by melatonin on ASA-induced histological alterations was more prominent when it was used after ASA in kidney and before ASA in testis. In this study, we demonstrated the beneficial effect of melatonin on high-dose ASA-related pathology of kidney and testis for the first time.

Purpose: The purpose of this study was to investigate the therapeutic and protective effects of molsidomine (MLS) against doxorubicin (DOX)-induced renal damage in rats. Methods: Forty rats were randomly divided into five groups (control, MLS, DOX, DOX+MLS and MLS+DOX groups). Thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO) and glutathione peroxidase (GPx) levels were determined from kidney tissues and blood urea nitrogen (BUN), creatinine (Cr) and albumin (Alb) levels also determined. Results: DOX treatment caused a significant increase in TBARS levels and a significant decrease in the GSH and CAT levels compared with the control group. In comparison, MLS administration before DOX injection caused a significant decrease in TBARS levels and also increases in GSH and CAT levels, whereas treatment of MLS after DOX injection did not show any beneficial effect on these parameters. All groups showed a significant increase in NO levels compared to the control group. There were no significant differences among the all groups for BUN and Cr levels. Serum level of Alb decreased in the DOX-treated groups when compared with control and MLS groups. The histopathological findings were in accordance with the biochemical results. MLS treatment reversed the DOX-induced kidney damage in group 4. MLS treatment before DOX injection exerted a protective effect against DOX-induced kidney damage. Conclusions: MLS shows promise as a possible therapeutic intervention for the prevention of kidney injury associated with DOX treatment. Additional studies are warranted.

yoldas, zeynep rumeysa/0000-0002-5608-9003 WOS: 000354606400024 PubMed: 24903065 Objective: To evaluate the influence of delivery mode on oxidative stress in human breast milk. Methods: Thirty-three women who delivered by vaginal birth and 55 women who underwent cesarean section (CS) were included in this study. Colostral samples were collected on the second day after delivery. Total antioxidative status (TAS), total oxidative status (TOS), oxidative stress index (OSI), malonyldialdehyde (MDA), and glutathione peroxidase (GSH-Px) levels were determined and compared. Results: Colostrum TAS was significantly higher in women of vaginal birth, than in women with CS (p

The aim of this study was to investigate the possible protective effects of melatonin and β-d-glucan against ischemia-reperfusion (IR) injury in rats.Forty rats were randomly divided into 5 groups, each consisting of 8 animals, as follows. Sham group [S], IR group [C], IR + β-Glucan group [β], IR + melatonin group [MLT], IR + melatonin + β-Glucan group [MLT + β]. The rats in the C, β, MLT and MLT + β groups were subjected to IR for 60 min each. Melatonin (10 mg∙kg⁻¹) was intraperitoneally injected for a single dose 30 min before IR. β-Glucan (50 mg∙kg⁻¹∙day⁻¹) was orally administered for 10 days to rats. All of the rats were killed on day 11, and histological changes in the liver and tissue levels of oxidants and antioxidants were evaluated.Malondialdehyde [MDA] level were significantly higher in the C group compared to the S group (p = 0.007). MDA level were significantly higher in the β group compared to the MLT and MLT + β groups (p =0.007). Tissue antioxidant markers (superoxide dismut ase [SOD], glutathione-peroxidase [GPx], and catalase [CAT]) were significantly lower in the C group than the S group (p0.05). SOD levels were simply not significant in the β group compared to the MLT and MLT + β groups. CAT and GPx activities were significantly higher in the β group compared to the MLT and MLT + β groups (p = 0.004).The histological damage ameliorated in β, MLT and MLT + β groups compared to C group.

Ischemia/reperfusion (IR) injury (IRI) in liver transplant patients may negatively affect graft function. Although β-glucan protects kidneys against IRI, its effect on the liver is unknown. This study sought to investigate β-glucan effects on oxidative damage to the liver after IRI in rats.Thirty-two rats were randomly divided into 4 experimental groups n = 8 in each group: sham, IR, β-glucan and IR + β-glucan. β-Glucan (50 mg.kg(-1) . day(-1)) was orally administered for 10 days to rats in the β-glucan and IR + β-glucan groups. The rats in the IR and IR + β-glucan groups were subjected to ischemia and reperfusion (IR) for 60 minutes each. All rats were killed on day 11 to evaluate histological changes as well as tissue levels of oxidants and antioxidants.Malondialdehyde (MDA) levels were significantly higher in the IR than the sham group (P = .001). MDA level was significantly higher in the IR group than in the IR + β-glucan group (P = .001). The levels of tissue antioxidant markers (superoxide dismutase [SOD], glutathione-peroxidase [GPx], and catalase [CAT]) were significantly lower in the IR group than in the sham group (P.05). SOD and GPx levels did not differ significantly between the IR and IR + β-glucan groups. CAT activity was significantly higher in the IR than the IR + β-glucan group (P = .001). Histological tissue damage was reduced in the IR + β-glucan than the IR group.Liver IRI is an inevitable problem during liver surgery. Our results suggested that β-glucan pretreatment suppressed oxidative stress and increased antioxidant levels in an rat model of liver IRI.