scholarly journals Oxidative stress in rat liver during acute cadmium and ethanol intoxication

2012 ◽  
Vol 77 (2) ◽  
pp. 159-176 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Milica Ninkovic ◽  
Danijela Vucevic ◽  
Ivan Boricic ◽  
...  

The aim of our study was to investigate the effects of binge drinking on prooxidant/antioxidant system in rat liver in acute cadmium (Cd) intoxication. In experiment male Wistar rats were used and divided into following groups: 1. control, 2. ethanol-treated group, in five subsequent doses of 2 g/kg administered by orogastric tube, 3. Cd-treated group in a single dose of 2.5 mg/kg intraperitoneally, 4. group that received Cd 12 hours after the last dose of ethanol. Blood and liver samples were collected for determination of oxidative stress parameters, 24 hours after treatment. When administered in combination, ethanol and Cd induced a more pronounced increase in serum and liver malondialdehyde level than either of these substances alone (p<0.01). Liver manganese superoxide dismutase (MnSOD) activity was increased both in ethanol and Cd-treated group (p<0.01), while liver copper/zinc superoxide dismutase (Cu/ZnSOD) activity was elevated in Cd group only. However, when administered in combination, ethanol and Cd induced a more pronounced decrease in liver MnSOD and Cu/ZnSOD activity 24 hours after treatment (p<0.01). Based on our study, it can be concluded that ethanol may act sinergistically with Cd in inducing lipid peroxidation and reduction in liver SOD activity.

2020 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Esfandiyar Heidari ◽  
Seyed Ali Hosseini ◽  
Mohammad Ali Azarbayjani

Background: The prevalence of anabolic steroids abuse in athletes and non-athletes is associated with the risk of injury to various organs, but there are limited studies of oxidative changes in kidney tissue following nandrolone (N) administration. Objectives: the aim of this study was to investigate the effect of N treatment with and without resistance training (RT) on superoxide dismutase (SOD) concentration and tissue pathology of kidney tissue in rats. Methods: In this experimental study, 20 male Wistar rats were randomly divided into four groups of five rats including 1) control (C), 2) sham (normal saline) (Sh), 3) N, and 4) N + RT. Groups 3 and 4 received 10 mg/kg N peritoneally, and the N + RT group performed 1 m ladder climbing for eight weeks and three sessions per week. SOD levels of kidney tissue were measured by ELISA and radioimmunoassay. Hematoxylin-eosin (H&E) staining was used to evaluate oxidative stress levels in kidney tissue. One-way ANOVA with Bonferroni’s post- hoc tests were used for analysis of research findings in SPSS version 22 (P ≤ 0.05). Results: SOD levels in the C group were higher than the Sh (P = 0.001), N (P = 0.001), and N + RT (P = 0.001) groups. SOD levels were lower in the Sh group than in the N (P = 0.049) and N + RT (P = 0.001) groups. However, there was no significant difference in SOD levels in the N + RT group and N group (P = 0.28). Also, oxidative stress levels were normal in tissue studies in all groups. Conclusions: It seems that Ntreatment with and without RT reduces SOD activity in kidney tissue, but more studies are needed in this regard given the normality of tissue oxidative stress results.


2010 ◽  
Vol 299 (2) ◽  
pp. F445-F452 ◽  
Author(s):  
Hua Lu ◽  
Junhui Zhen ◽  
Tianfu Wu ◽  
Ai Peng ◽  
Ting Ye ◽  
...  

Oxidative stress plays an important role in the pathogenesis of anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM-GN). Superoxide dismutase (SOD) is the first line of defense against oxidative stress by converting superoxide to hydrogen peroxide (H2O2). We investigated the effect of the SOD mimetic drug tempol on anti-GBM-GN in mice. 129/svJ mice were challenged with rabbit anti-mouse-GBM sera to induce GN and subsequently divided into tempol (200 mg·kg−1·day−1, orally) and vehicle-treated groups. Routine histology, SOD and catalase activities, malondialdehyde (MDA), H2O2, and immunohistochemical staining for neutrophils, lymphocytes, macrophages, p65-NF-κB, and osteopontin were performed. Mice with anti-GBM-GN had significantly reduced renal SOD and catalase activities and increased H2O2 and MDA levels. Unexpectedly, tempol administration exacerbated anti-GBM-GN as evidenced by intensification of proteinuria, the presence of severe crescentic GN with leukocyte influx, and accelerated mortality in the treated group. Tempol treatment raised SOD activity and H2O2 level in urine, upregulated p65-NF-κB and osteopontin in the kidney, but had no effect on renal catalase activity. Thus tempol aggravates anti-GBM-GN by increasing production of H2O2 which is a potent NF-κB activator and as such can intensify inflammation and renal injury. This supposition is supported by increases seen in p65-NF-κB, osteopontin, and leukocyte influx in the kidneys of the tempol-treated group.


1993 ◽  
Vol 265 (6) ◽  
pp. E839-E844 ◽  
Author(s):  
H. Kondo ◽  
I. Nakagaki ◽  
S. Sasaki ◽  
S. Hori ◽  
Y. Itokawa

To clarify the mechanism of oxidative stress in skeletal muscle atrophied by immobilization, we measured the activities of antioxidant enzymes and xanthine oxidase (XOD) and carried out the cytochemical study of hydrogen peroxide in a typical slow red muscle, the soleus. Male Wistar rats (15 wk old), of which ankle joints of one hindlimb were immobilized in the fully extended position, were killed after 4, 8, or 12 days. The activities of Mn-containing superoxide dismutase (Mn-SOD), Cu-Zn-containing superoxide dismutase (Cu-Zn-SOD), Se-dependent glutathione peroxidase (Se-GSHPx), glutathione S-transferase, catalase, and glutathione reductase were measured spectrophotometrically. The XOD activity and the concentrations of hypoxanthine, xanthine, and urate were measured using a high-performance liquid chromatography. The cytochemical study of hydrogen peroxide in short-term organ culture was performed using an electron microscope. Increased Cu-Zn-SOD and decreased Mn-SOD in atrophy might reflect increased generation of superoxide anions in the cytoplasm rather than in the mitochondria. The source of superoxide anions in the cytoplasm might be the increased superoxide-producing XOD. Enhanced generation of superoxide anions and increased Cu-Zn-SOD activity in atrophy suggested the enhanced generation of hydrogen peroxide in the cytoplasm. Due to the unchanged activity of Se-GSHPx and the unchanged or slightly increased activity of catalase in atrophy, the ability to degrade hydrogen peroxide might not increase so much. Hence, hydrogen peroxide is expected to be increased in atrophy. The cytochemical study supported this expectation.(ABSTRACT TRUNCATED AT 250 WORDS)


2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Catalina Martinez-Campos ◽  
Eleazar Lara-Padilla ◽  
Rosa Amalia Bobadilla-Lugo ◽  
Robert David Kross ◽  
Cleva Villanueva

Oxidative stress (OS) induced by acute exercise is reduced by chronic exercise. Ozone (O3) exposure produces OS. The aim of this study was to determine if aerobic exercise (AE) reduced OS produced by O3. A pilot experiment was performed with male Wistar rats submitted to AE (trained to swim 90 min/day). Adaptation to exercise was demonstrated three weeks after training by means of changes in reduced nitrates (NOx) in plasma. Therefore, two-week training was chosen for the following experiments. Six of twelve trained rats were exposed to O3(0.5 ppm, 4 h/day, one hour before exercise). Two groups of sedentary animals (n=6each) were used as controls, one of which was exposed to O3. At the end of the experiments NOx, 8-isoprostane (8-IP), malondialdehyde (MDA), superoxide dismutase (SOD) activity, and carbonyls (CBs) were measured in plasma. CBs did not change in any group. O3-induced OS was manifested by reduced NOxand SOD activity, as well as increased 8-IP and MDA. Exercise significantly blocked O3effects although SOD was also decreased by exercise (a greater drop occurring in the O3group). It is concluded that AE protects against OS produced by O3and the effect is independent of SOD.


2013 ◽  
Vol 78 (2) ◽  
pp. 179-195 ◽  
Author(s):  
Dusan Mladenovic ◽  
Milica Ninkovic ◽  
Danijela Vucevic ◽  
Miodrag Colic ◽  
Marjan Micev ◽  
...  

The aim of our study was to investigate the effects of binge drinking on paracetamol induced oxidative stress in mice liver. Male Swiss mice were divided into groups: control; ethanol-treated group (E) in five subsequent doses of 2 g/kg by orogastric tube; paracetamol-treated group (P) in a dose of 300 mg/kg intraperitoneally; group that received paracetamol 12 hrs after the last dose of ethanol (PE). Blood and liver samples were collected for determination of oxidative stress parameters 6, 24 and 48 hrs after treatment. Prior binge drinking potentiated paracetamol-induced rise in liver malondialdehyde level 48 hours after treatment in comparison with P and E groups (17.14 ? 1.98 vs 13.14 ? 0.82 and 12.99 ? 1.18 ?mol/L, p<0.01). Ethanol and paracetamol in combination induced a more pronounced decrease in liver GSH level than either of these substances alone at all time intervals (p<0.01). Total liver superoxide dismutase (SOD) activity was significantly lower in PE 48 hours after treatment in comparison with P and E groups (251.73 ? 80.63 vs 707.62 ? 179.92 and 1179.62 ? 147.94 U/mg prot., p<0.01). The lowest MnSOD activity in PE group was detected 48 hrs after treatment (86.52 ? 28.31; 41.13 ? 11.07 and 23.16 ? 5.18 U/mg prot. in P, E and PE groups, p<0.05, respectively). Prior binge ethanol drinking potentiates paracetamol-induced reduction of antioxidative capacity of hepatocytes due to GSH depletion and SOD activity reduction, simultaneously increasing lipid peroxidation caused by paracetamol.


Author(s):  
Elena Rodríguez-Sánchez ◽  
José Alberto Navarro-García ◽  
Jennifer Aceves-Ripoll ◽  
Laura González-Lafuente ◽  
Nerea Corbacho-Alonso ◽  
...  

Abstract Aging and chronic kidney disease (CKD) are important interrelated cardiovascular risk (CVR) factors linked to oxidative stress, but this relationship has not been well studied in older adults. We assessed the global oxidative status in an older population with normal to severely impaired renal function. We determined the oxidative status of 93 older adults (mean age 85 years) using multimarker scores. OxyScore was computed as index of systemic oxidative damage by analyzing carbonyl groups, oxidized low-density lipoprotein, 8-hydroxy-2′-deoxyguanosine, and xanthine oxidase activity. AntioxyScore was computed as index of antioxidant defense by analyzing catalase and superoxide dismutase (SOD) activity and total antioxidant capacity. OxyScore and AntioxyScore were higher in subjects with estimated glomerular filtration rate (eGFR) &lt;60 mL/min/1.73 m2 than in peers with eGFR &gt;60 mL/min/1.73 m2, with protein carbonyls, catalase, and SOD activity as major drivers. Older adults with a recent cardiovascular event had similar OxyScore and AntioxyScore as peers with eGFR &gt;60 mL/min/1.73 m2. Multivariate linear regression analysis revealed that both indices were associated with decreased eGFR independently of traditional CVR factors. Interestingly, AntioxyScore was also associated with diuretic treatment, and a more pronounced increase was seen in subjects receiving combination therapy. The associations of AntioxyScore with diuretic treatment and eGFR were mutually independent. In conclusion, eGFR is the major contributor to the imbalance in oxidative stress in this older population. Given the association between oxidative stress, CKD, and CVR, the inclusion of renal function parameters in CVR estimators for older populations, such as the SCORE-OP, might improve their modest performance.


Author(s):  
Kiptiyah Kiptiyah ◽  
Widodo Widodo ◽  
Gatot Ciptadi ◽  
Aulanni’am Aulanni’Am ◽  
Mohammad A. Widodo ◽  
...  

AbstractBackgroundWe investigated whether 10-gingerol is able to induce oxidative stress in cumulus cells.MethodsFor the in-vitro research, we used a cumulus cell culture in M199, containing 10-gingerol in various concentrations (0, 12, 16, and 20 µM), and detected oxidative stress through superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentrations, with incubation periods of 24, 48, 72, and 96 h. The obtained results were confirmed by in-silico studies.ResultsThe in-vitro data revealed that SOD activity and MDA concentration increased with increasing incubation periods: SOD activity at 0 µM (1.39 ± 0.24i), 12 µM (16.42 ± 0.35ab), 16 µM (17.28 ± 0.55ab), 20 µM (17.81 ± 0.12a), with a contribution of 71.1%. MDA concentration at 0 µM (17.82 ± 1.39 l), 12 µM (72.99 ± 0.31c), 16 µM (79.77 ± 4.19b), 20 µM (85.07 ± 2.57a), with a contribution of 73.1%. Based on this, the in-silico data uncovered that 10˗gingerol induces oxidative stress in cumulus cells by inhibiting HTR1A functions and inactivating GSK3B and AKT˗1.Conclusions10-gingerol induces oxidative stress in cumulus cells through enhancing SOD activity and MDA concentration by inhibiting HTR1A functions and inactivating GSK3B and AKT˗1.


Zygote ◽  
2019 ◽  
Vol 27 (6) ◽  
pp. 432-435
Author(s):  
Thais Rose dos Santos Hamilton ◽  
Gabriela Esteves Duarte ◽  
José Antonio Visintin ◽  
Mayra Elena Ortiz D’Ávila Assumpção

SummaryLong-term heat stress (HS) induced by testicular insulation generates oxidative stress (OS) on the testicular environment; consequently activating antioxidant enzymes such as superoxide dismutase (SOD), glutathione reductase (GR) and glutathione peroxidase (GPx). The aim of this work was to immunolocalize antioxidant enzymes present in different cells within the seminiferous tubule when rams were submitted to HS. Rams were divided into control (n = 6) and treated group (n = 6), comprising rams subjected to testicular insulation for 240 h. After the testicular insulation period, rams were subjected to orchiectomy. Testicular fragments were submitted to immunohistochemistry for staining against SOD, GR and GPx enzymes. We observed immunolocalization of GPx in more cell types of the testis after HS and when compared with other enzymes. In conclusion, GPx is the main antioxidant enzyme identified in testicular cells in an attempt to maintain oxidative balance when HS occurs.


2017 ◽  
Vol 45 (08) ◽  
pp. 1613-1629 ◽  
Author(s):  
Yan-Jiao Xu ◽  
Zao-Qin Yu ◽  
Cheng-Liang Zhang ◽  
Xi-Ping Li ◽  
Cheng-Yang Feng ◽  
...  

The present study was designed to assess the effects and potential mechanisms of ginsenosides on 17[Formula: see text]-ethynyelstradiol (EE)-induced intrahepatic cholestasis (IC). Ginsenoside at doses of 30, 100, 300[Formula: see text]mg/kg body weight was intragastrically (i.g.) given to rats for 5 days to examine the effect on EE-induced IC. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bile acid (TBA) were measured. Hepatic malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. Protein expression of proinflammatory cytokines TNF-[Formula: see text], IL-6 and IL-1[Formula: see text] was analyzed by immunohistochemistry and Western blot. Results indicated that ginsenosides remarkably prevented EE-induced increase in the serum levels of AST, ALT, ALP and TBA. Moreover, the elevation of hepatic MDA content induced by EE was significantly reduced, while hepatic SOD activities were significantly increased when treated with ginsenosides. Histopathology of the liver tissue showed that pathological injuries were relieved after treatment with ginsenosides. In addition, treatment with ginsenosides could significantly downregulate the protein expression of TNF-[Formula: see text], IL-6 and IL-1[Formula: see text] compared with EE group. These findings indicate that ginsenosides exert the hepatoprotective effect on EE-induced intrahepatic cholestasis in rats, and this protection might be attributed to the attenuation of oxidative stress and inflammation.


2017 ◽  
Vol 118 (8) ◽  
pp. 589-597 ◽  
Author(s):  
Emilce E. Llopart ◽  
Raúl E. Cian ◽  
Muñoz María Elvira López-Oliva ◽  
Ángela Zuleta ◽  
Adriana Weisstaub ◽  
...  

AbstractColonic effects of extruded whole-grain sorghum diets were evaluated using a model of growing rats. In all, twenty-four male Wistar rats were fed control (C), extruded white sorghum (EWS) or red sorghum (ERS). Consumption of sorghum diets showed satiety properties, with reduction of caecal pH, and lower activity ofβ-glucosidase andβ-glucuronidase enzymes. Decreased copper zinc superoxide dismutase and manganese superoxide dismutase and increased catalase and glutathione peroxidase levels were observed in colonic mucosa. The induction of antioxidant enzymes occurred through the activation of the nuclear factor erythroid 2-related factor 2 protein and its subsequent translocation into the nucleus. ERS was able to decrease the proliferation of proximal mucosa of colon, demonstrating a possible effect against colorectal tumourigenesis. EWS increased proliferation and also apoptosis, ensuring the re-establishment of homoeostasis of the colonic mucosa. No antioxidant systemic effect (serum or hepatic level) was observed. It is likely that despite the extrusion the low bioavailability of the phenolic compounds of sorghum diets caused them to exert mainly acute effects at the colon level. Extruded whole-grain sorghum is a good functional ingredient that might be promising in dietary prevention of intestinal diseases.


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