Antioxidative effect of DJ-1 is enhanced in NG108-15 cells by DPMQ induced copper influx

2020 ◽  
Author(s):  
Ting-Yu Chin ◽  
Che-Chuan Wang ◽  
Kuo-Hsing Ma ◽  
Chia-Wei Kuo ◽  
Ming-Kuan Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Nuclear Translocation ◽  
Cellular Level ◽  
Dependent Manner ◽  
Copper Binding ◽  
Antioxidative Effect ◽  
Sod Activity ◽  
Redox Imbalance ◽  
Endogenous Proteins

Disruption of copper homeostasis is closely involved in neurodegenerative disorders. This study examined whether a hybrid copper binding compound, (E)-2-(4-(dimethylamino)phenylimino)methyl)quinolin-8-ol (DPMQ), is able to protect NG108-15 cells against oxidative stress. we found that treatment of cells with rotenone or hydrogen peroxide increased cellular oxidative stress and resulted in mitochondrial dysfunction and apoptosis. The cellular levels of Nrf2 and the Cu2+ chaperone DJ-1 were also decreased. These oxidative detrimental effects were all inhibited when cells were co-treated with DPMQ. DPMQ increased cellular Cu2+ content, DJ-1 protein level, superoxide dismutase (SOD) activity and Nrf2 nuclear translocation under basal state. The activity of SOD decreased under redox imbalance and this decrease was blocked by DPMQ treatment, while the protein level of SOD1 remained unaltered regardless of the oxidative stress and DPMQ treatment. Using endogenous proteins, co-immunoprecipitation showed that DJ-1 bound with SOD1 and Nrf2 individually. The amount of Nrf2, bound to DJ-1, consistently reflected its cellular level, while the amount of SOD1, bound to DJ-1, was potentiated by DPMQ, being greater in basal state than under redox imbalance. Simultaneous inclusion of non-permeable Cu2+ chelator tetrathiomolybdate or triethylenetetramine during DPMQ treatment blocked all aforementioned effects of DPMQ, showing that the dependency of the effect of DPMQ on extracellular Cu2+. In addition, silencing of DJ-1 blocked the protection of DPMQ against oxidative stress. Taken all together, our results suggest that DPMQ stabilizes DJ-1 in a Cu2+ dependent manner, which then brings about SOD1 activation and Nrf2 nuclear translocation; these together alleviate cellular oxidative stress.

scholarly journals Mini-GAGR, an intranasally applied polysaccharide, activates the neuronal Nrf2-mediated antioxidant defense system

2018 ◽  
Vol 293 (47) ◽  
pp. 18242-18269 ◽  
Author(s):  
Kelsey Murphy ◽  
Killian Llewellyn ◽  
Samuel Wakser ◽  
Josef Pontasch ◽  
Natasha Samanich ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant System ◽  
Cortical Neurons ◽  
Hippocampal Neurons ◽  
Nuclear Translocation ◽  
Growth Factor Receptor ◽  
Antioxidant Defense System ◽  
Related Factor ◽  
Dependent Manner ◽  
Amyloid Aβ

Oxidative stress triggers and exacerbates neurodegeneration in Alzheimer's disease (AD). Various antioxidants reduce oxidative stress, but these agents have little efficacy due to poor blood–brain barrier (BBB) permeability. Additionally, single-modal antioxidants are easily overwhelmed by global oxidative stress. Activating nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) and its downstream antioxidant system are considered very effective for reducing global oxidative stress. Thus far, only a few BBB-permeable agents activate the Nrf2-dependent antioxidant system. Here, we discovered a BBB-bypassing Nrf2-activating polysaccharide that may attenuate AD pathogenesis. Mini-GAGR, a 0.7-kDa cleavage product of low-acyl gellan gum, increased the levels and activities of Nrf2-dependent antioxidant enzymes, decreased reactive oxygen species (ROS) under oxidative stress in mouse cortical neurons, and robustly protected mitochondria from oxidative insults. Moreover, mini-GAGR increased the nuclear localization and transcriptional activity of Nrf2 similarly to known Nrf2 activators. Mechanistically, mini-GAGR increased the dissociation of Nrf2 from its inhibitor, Kelch-like ECH-associated protein 1 (Keap1), and induced phosphorylation and nuclear translocation of Nrf2 in a protein kinase C (PKC)- and fibroblast growth factor receptor (FGFR1)-dependent manner. Finally, 20-day intranasal treatment of 3xTg-AD mice with 100 nmol of mini-GAGR increased nuclear p-Nrf2 and growth-associated protein 43 (GAP43) levels in hippocampal neurons, reduced p-tau and β-amyloid (Aβ) peptide–stained neurons, and improved memory. The BBB-bypassing Nrf2-activating polysaccharide reported here may be effective in reducing oxidative stress and neurodegeneration in AD.

Early Biomarkers for the Anti-Angiogenic and Anti-Tumor Activity of the Superoxide Dismutase 1 (SOD1) Inhibitor Tetrathiomolybdate.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4214-4214
Author(s):  
M.J. Braunstein ◽  
E. Smith ◽  
C. Timucin ◽  
F. Doñate ◽  
J.C. Juarez ◽  
...  
Keyword(s):  
Blood Cell ◽  
Animal Studies ◽  
Drug Effects ◽  
Dependent Manner ◽  
Copper Binding ◽  
Endothelial Progenitor ◽  
Sod Activity ◽  
Color Flow ◽  
Inhibition Of Angiogenesis

Abstract Background: Identifying biomarkers that monitor clinical response to cancer therapies is crucial. Tetrathiomolybdate (TM) is a highly specific, high-affinity, orally available copper-binding compound that inhibits CuZn SOD1, leading to robust anti-angiogenic and anti-tumor effects. TM is currently being evaluated in Phase II cancer trials including for relapsed and refractory multiple myeloma (MM). TM’s inhibition of angiogenesis has been attributed to depletion of systemic Cu, which is known to affect multiple key angiogenesis regulators; however, in mice, inhibition of angiogenesis by TM occurred before a measurable decrease in systemic Cu. We have recently shown that in MM, circulating endothelial progenitor cell (EPC) levels serve as a reliable biomarker of disease severity which covaries with tumor load and disease progression. Furthermore, recent evidence from our laboratory and by others indicates that EPCs display evidence of clonality and are genetically related to MM cells. In the present study, the relationship between anti-angiogenic and anti-SOD1 activities of TM were compared by determining its effects on: circulating endothelial progenitor cells (EPCs) in bonnet macaques (M. radiata); on angiogenesis and SOD1 activity in blood cells from mice and humans. Methods: TM was manufactured with >99% purity using a proprietary process (choline salt: ATN-224). For animal studies, three female and three male young adult monkeys were treated with TM (0.5 mg/kg, s.c.) daily for 22 days, followed by a 26 day drug holiday, and a second course of drug. Blood was drawn from the cephalic vein, separated by Ficoll, and red cell lysis. EPCs were identified as CD31+/CD133+/CD45− weak cells using 3-color flow cytometry. For SOD activity, blood from normal control subjects was incubated with TM for 5.5 hr at 37°C. SOD activity was measured in 30 μg of protein from treated blood pellets using an SOD Activity Kit. Results: Administration of TM to the monkeys resulted in a rapid, profound, and reversible decrease in circulating EPCs without significant toxicity. The levels of EPCs increased initially at day 6 in 5 of the 6 subjects, and then decreased to 7% of baseline at day 21. The EPC levels rebounded to normal levels once treatment was discontinued and dropped again after treatment was reinstated. Other hematopoietic parameters (RBC, WBC, platelet counts, and hemoglobin) were not affected by treatment. Although we did not measure blood cell SOD in the macaque study, substantial inhibition of blood cell SOD is associated with hematologic toxicities which did not occur in these animals, suggesting that RBC SOD activity is inhibited at higher doses than those needed for anti-angiogenic activity. TM treatment inhibited SOD activity in blood cell pellets obtained from human controls in a dose dependent manner, with an IC50 3 μM. Conclusion: These results show, for the first time, that in vivo effects of TM include suppression of circulating EPC levels. Since circulating EPCs are genetically related to tumor cells in MM, at least the anti-MM effects of TM may depend on its suppressive effects on EPCs as well as on angiogenesis in general. Furthermore, EPCs are a sensitive indicator of TM actions since their reversible modulation correlated with drug therapy. Lastly, macaques may represent a reliable model of human response to determine drug effects on EPCs and angiogenesis.

scholarly journals Safranal Treatment Improves Hyperglycemia, Hyperlipidemia and Oxidative Stress in Streptozotocin-Induced Diabetic Rats

2013 ◽  
Vol 16 (2) ◽  
pp. 352 ◽  
Author(s):  
Saeed Samarghandian ◽  
Abasalt Borji ◽  
Mohammad Bagher Delkhosh ◽  
Fariborz Samini
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Antioxidant Properties ◽  
Diabetic Rats ◽  
Dependent Manner ◽  
Protective Effects ◽  
Total Lipids ◽  
Sod Activity ◽  
Chemically Induced ◽  
Antioxidant Defense Systems

Purpose. Clinical research has confirmed the efficacy of several plant extracts in the modulation of oxidative stress associated with diabetes mellitus. Findings indicate that safranal has antioxidant properties. The aim of the present study was the evaluation of possible protective effects of safranal against oxidative damage in diabetic rats. Methods. In this study, the rats were divided into the following groups of 8 animals each: control, untreated diabetic, three safranal (0.25, 0.50, 0.75 mg/kg/day)-treated diabetic groups. Diabetes was induced by streptozotocin (STZ) in rats. STZ was injected intraperitoneally at a single dose of 60 mg/kg for diabetes induction. Safranal (intraperitoneal injection) was administered 3 days after STZ administration; these injections were continued to the end of the study (4 weeks). At the end of the 4-week period, blood was drawn for biochemical assays. In order to determine the changes of cellular antioxidant defense systems, antioxidant enzymes including glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were measured in serum. Moreover we also measured serum nitric oxide (NO) and serum malondialdehyde (MDA) levels, a marker of lipid peroxidation.  Results. STZ-induced diabetes caused an elevation (p < 0.001) of blood glucose, MDA, NO, total lipids, triglycerides and cholesterol, with reduction of GSH level and CAT and SOD activities. The results indicated that the significant elevation in the blood glucose, MDA, NO, total lipids, triglycerides, cholesterol and reduction of glutathione level and CAT and SOD activity were ameliorated in the safranal–treated diabetic groups compared with the untreated groups, in a dose dependent manner (p < 0.05, p<0.01, p < 0.001). Conclusion. These results suggest that safranal has antioxidant properties and improves chemically-induced diabetes and its complications by modulation of oxidative stress. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

scholarly journals Upregulation of UCP2 Expression Protects against LPS-Induced Oxidative Stress and Apoptosis in Cardiomyocytes

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jinda Huang ◽  
Wanwan Peng ◽  
Yijun Zheng ◽  
Hu Hao ◽  
Sitao Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cytochrome C ◽  
Protein Level ◽  
Caspase 3 ◽  
Uncoupling Protein ◽  
Dependent Manner ◽  
Mitochondrial Cytochrome ◽  
Protein Levels ◽  
Ucp2 Expression ◽  
Mitochondrial Cytochrome C

Uncoupling protein 2 (UCP2) has a cardioprotective role under septic conditions, but the underlying mechanism remains unclear. This study aimed at investigating the effects of UCP2 on the oxidative stress and apoptosis of cardiomyocytes induced by lipopolysaccharide (LPS). First, LPS increased UCP2 expression in cardiomyocytes in a time-dependent manner. LPS increased the production of lactate dehydrogenase (LDH), reactive oxygen species (ROS), and malondialdehyde (MDA) and decreased the level of superoxide dismutase (SOD). However, UCP2 knockdown increased the LPS-induced cardiac injury and oxidative stress. In addition, LPS damaged the mitochondrial ultrastructure and led to the disruption of mitochondrial membrane potential (MMP), as well as the release of mitochondrial cytochrome c. UCP2 knockdown aggravated mitochondrial injury and the release of mitochondrial cytochrome c. LPS increased the protein levels of Bax and cleaved-caspase-3, decreased the protein level of Bcl-2, and upregulated the protein level of mitogen-activated protein kinase. However, upon UCP2 knockdown, the protein levels of Bax and cleaved-caspase-3 increased even further, and the protein level of Bcl-2 was further decreased. The protein level of phosphorylated p38 was also further enhanced. Thus, UCP2 protects against LPS-induced oxidative stress and apoptosis in cardiomyocytes.

scholarly journals Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiaopeng Tian ◽  
Chunhong Zhao ◽  
Jinbo Guo ◽  
Shurui Xie ◽  
Fengrong Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bile Duct ◽  
Hepatic Fibrosis ◽  
Transforming Growth Factor ◽  
Bile Duct Ligation ◽  
Antioxidant Properties ◽  
Dependent Manner ◽  
Sod Activity ◽  
Duct Ligation ◽  
Clinical Benefits

Background.The sympathetic nervous system (SNS) is responsible for hepatic stellate cells (HSCs) activation and the accumulation of collagen that occurs in hepatic fibrogenesis. Carvedilol has been widely used for the complication of hepatic cirrhosis in the clinic. Furthermore, it has powerful antioxidant properties. We assessed the potential antifibrotic effects of carvedilol and the underlying mechanisms that may further enhance its clinical benefits.Methods.Using a bile duct ligation rat model of hepatic fibrosis, we studied the effects of carvedilol on the fibrosis, collagen deposition, and oxidative stress based on histology, immunohistochemistry, western blot, and RT-PCR analyses.Results.Carvedilol attenuated liver fibrosis, as evidenced by reduced hydroxyproline content and the accumulation of collagen, downregulated TIMP-1 and TIMP-2, and upregulated MMP-13. MMP-2 was an exception, which was decreased after carvedilol treatment for 2 weeks and upregulated after carvedilol treatment for 4 weeks. Carvedilol reduced the activation of HSCs, decreased the induction of collagen, transforming growth factor-β1, and MDA content, and strengthened the SOD activity. The antifibrotic effects were augmented as dosages increased.Conclusions.The study indicates that carvedilol attenuated hepatic fibrosis in a dose-dependent manner. It can decrease collagen accumulation and HSCs activation by the amelioration of oxidative stress.

scholarly journals The Role of Nrf2 Transcription Factor and Sp1-Nrf2 Protein Complex in Glutamine Transporter SN1 Regulation in Mouse Cortical Astrocytes Exposed to Ammonia

2021 ◽  
Vol 22 (20) ◽  
pp. 11233
Author(s):  
Katarzyna Dąbrowska ◽  
Katarzyna Skowrońska ◽  
Mariusz Popek ◽  
Jan Albrecht ◽  
Magdalena Zielińska
Keyword(s):  
Protein Level ◽  
Nuclear Translocation ◽  
Mapk Pathway ◽  
Ammonia Toxicity ◽  
Dependent Manner ◽  
Glutamine Transporter ◽  
The Brain ◽  
Nrf2 Protein ◽  
Glutamine Uptake

Ammonia toxicity in the brain primarily affects astrocytes via a mechanism in which oxidative stress (OS), is coupled to the imbalance between glutamatergic and GABAergic transmission. Ammonia also downregulates the astrocytic N system transporter SN1 that controls glutamine supply from astrocytes to neurons for the replenishment of both neurotransmitters. Here, we tested the hypothesis that activation of Nrf2 is the process that links ammonia-induced OS formation in astrocytes to downregulation and inactivation of SN1 and that it may involve the formation of a complex between Nrf2 and Sp1. Treatment of cultured cortical mouse astrocytes with ammonia (5 mM NH4Cl for 24 h) evoked Nrf2 nuclear translocation, increased its activity in a p38 MAPK pathway-dependent manner, and enhanced Nrf2 binding to Slc38a3 promoter. Nrf2 silencing increased SN1 mRNA and protein level without influencing astrocytic [3H]glutamine transport. Ammonia decreased SN1 expression in Nrf2 siRNA treated astrocytes and reduced [3H]glutamine uptake. In addition, while Nrf2 formed a complex with Sp1 in ammonia-treated astrocytes less efficiently than in control cells, treatment of astrocytes with hybrid-mode inactivated Sp1-Nrf2 complex (Nrf2 silencing + pharmacological inhibition of Sp1) did not affect SN1 protein level in ammonia-treated astrocytes. In summary, the results document that SN1 transporter dysregulation by ammonia in astrocytes involves activation of Nrf2 but does not require the formation of the Sp1-Nrf2 complex.

scholarly journals Expression and activity of superoxide dismutase isoenzymes in colorectal cancer.

2009 ◽  
Vol 56 (4) ◽  
Author(s):  
Michał Skrzycki ◽  
Monika Majewska ◽  
Małgorzata Podsiad ◽  
Hanna Czeczot
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Lipid Peroxidation ◽  
Protein Level ◽  
Cancer Development ◽  
Colorectal Cancers ◽  
Sod Activity ◽  
Colorectal Cancer Cells ◽  
Nf Kappab ◽  
Expression And Activity

The aim of the study was an evaluation of changes in protein level and activity of SOD isoenzymes, and the participation of AP-1 and NF-kappaB in subsequent stages of colorectal cancer development. Studies were conducted on 65 colorectal cancers. Controls were unchanged colon regions. Activity of SOD isoenzymes, lipid peroxidation level (TBARS), and protein level of SOD1, SOD2, AP-1 and NF-kappaB were determined. We found that the protein level and activity of SOD isoenzymes and protein level of AP-1 and NF-kappaB change in subsequent stages of clinical advancement of colorectal cancer, according to UICC (I-IV), and in grades of tumor cells differentiation (G(1)-G(3)). These results indicate adaptation of colorectal cancer cells to oxidative stress, and show that the observed changes of SOD activity and protein level depend on gradual progression of colorectal cancer, and suggest an impairment of processes regulated by AP-1 and NF-kappaB which are critical for tumor progression (proliferation, differentiation and apoptosis).

scholarly journals The Antioxidant and Anti-Inflammatory Effects of Quercus brantii Extract on TNBS-Induced Ulcerative Colitis in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Mahvash Alizade Naini ◽  
Shayan Mehrvarzi ◽  
Asal Zargari-Samadnejadi ◽  
Nader Tanideh ◽  
Mohammad Ghorbani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Body Weight Loss ◽  
Trinitrobenzene Sulfonic Acid ◽  
High Morbidity ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Sod Activity ◽  
Anti Inflammatory ◽  
Quercus Brantii

Objectives. Ulcerative colitis is a common subtype of persistent inflammatory bowel disease with high morbidity consequences. Despite unknown definite pathogenesis, multiple anti-inflammatory medications are used for its treatment. Traditionally, Quercus brantii (QB), mostly available in the Middle East, has been used for gastrointestinal disorders. Other beneficial effects associated with QB include reduction of oxidative stress, inflammations, homeostatic instability, and improvement in clinical conditions. Materials and Methods. This experimental study was designed to assess the possible therapeutic effects of QB on UC and compare its effects with those of sulfasalazine. Of the 70 Wistar rats clustered in seven groups, ten received only alcohols and sixty were confirmed to be suffering from trinitrobenzene sulfonic acid- (TNBS-) induced colitis. Four groups received different dosages of QB extract via oral and rectal routes, one received sulfasalazine, and the other remaining two groups received nothing. The effects of QB were evaluated by assessing macroscopic and histologic scoring, measuring inflammatory mediators, and determining oxidative stress markers. Results. Comparing to the untreated TNBS-induced control groups, QB-treated groups showed a dose- and route-dependent improvement comparable with sulfasalazine. Treating rats with QB reduced the microscopic and macroscopic damage, decreased TNF-α, IL-6, NO, MPO activity, and MDA content, increased superoxide dismutase (SOD) activity, and reduced body weight loss. Conclusions. Our data recommended the anti-inflammatory and antioxidant effects of QB extract in a dose-dependent manner.

Sufentanil Affects High Glucose-Induced Oxidative Stress in and Apoptosis of Cardiomyocytes by Regulation of miR-142-3p Expression

2021 ◽  
Vol 11 (3) ◽  
pp. 466-470
Author(s):  
Zhiyong Liu ◽  
Cuiqing Ding ◽  
Changqing Yao ◽  
Jinhui Chen
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Mda Content

To explore the effects and molecular mechanisms of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes, cardiomyocytes H9c2 cells were classified into groups based on different treatments as high-glucose (HG), HG with low, medium, or high-dose sufentanil, HG with high-dose sufentanil and anti-miR-NC, HG with high-dose sufentanil and anti-miR-142-3p, and control. The cells’ superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected using respective kits. The apoptosis rate in each group was detected by flow cytometry. The expressions of cleaved caspase-3 and pro-caspase3 were determined using western blotting. The expression of miR-142-3p in cardiomyocytes was detected using real-time fluorescent quantitative PCR. Compared with the control group, the HG group had decreased SOD activity, pro-caspase-3 expression, and miR-142-3p expression and increased MDA content, apoptosis, and cleaved caspase-3 expression (P < 0.05). Compared with the HG group, the SOD activity and pro-caspase-3 expression increased and the MDA content, apoptosis rate, and cleaved caspase-3 expression decreased in HG cells treated with low, medium, or high-dose sufentanil. The expression of miR-142-3p was increased in a dose-dependent manner (P < 0.05). The interference of miR-142-3p reversed the effect of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes. Sufentanil may inhibit high glucose-induced oxidative stress in and apoptosis of cardiomyocytes by upregulating miR-142-3p expression.

Status of Oxidative Stress in Cerebral Cortex and Testes, Acetylcholinesterase Activity in Cerebral Cortex and Sperm Parameters in Cadmium-Exposed Rats

2019 ◽  
Author(s):  
C. N Makwana ◽  
S. S. Rao ◽  
U. D. Patel ◽  
C. M. Modi ◽  
H. B. Patel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Sperm Count ◽  
Acetylcholinesterase Activity ◽  
Cadmium Exposure ◽  
Dependent Manner ◽  
Epididymal Sperm ◽  
Sod Activity ◽  
Dose Dependent ◽  
Ppm Level

The present study was carried out to evaluate oxidative stress mediated pathophysiological alterations in brain cerebral cortex and testes of rats exposed to cadmium chloride at 15, 50 and 100 ppm in drinking water for 28 days. The activity of SOD in brain of rats of all toxicity groups was non- significantly decreased. The SOD activity in testes was significantly decreased in animals exposed to 50 and 100 ppm level of cadmium. The catalase activity in brain cerebral cortex and testes was significantly decreased in dose dependent manner. The GSH levels in brain and testes tissue were increased at all tested levels of exposure of cadmium. The acetylcholinesterase activity in brain of rats exposed all levels of Cd were significantly decreased. Cadmium exposure at 100 ppm level significantly reduced the total epididymal sperm count. However, the epididymal sperm motility was significantly reduced in rats exposed to all tested levels of cadmium. The different levels of cadmium exposure produced pathological lesions in brain cerebral cortex and testes which were remarkable at 100 ppm level of exposure as compared to other levels of exposure in rats. In conclusion, cadmium exposure at 100 ppm for 28 days in rats produced marked alterations in both brain and testes through oxidative insult.

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