RETRACTED: Cadmium induced cardiac oxidative stress in rats and its attenuation by GSP through the activation of Nrf2 signaling pathway

Nazimabashir,; Manoharan, Vaihundam; Miltonprabu, Selvaraj

doi:10.1016/j.cbi.2015.10.005

Cited by 56 publications

(29 citation statements)

References 61 publications

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“…Our results show that cadmium decreases Nrf2 mRNA levels as well as the transcription of Nrf2-induced downstream target genes (phase 2 genes) (Figure 4), suggesting that cadmium-induced oxidative stress accelerates gene transcription significantly ( p < 0.01). Previous studies have shown that Cd exposure causes a marked increase in the generation of reactive oxygen species (ROS) that exceed the physiological capacity of the antioxidant enzyme, finally exhausting these enzymes, reducing their activity, and thereby decrease the activity of Nrf2 [43,44]. In our experimental conditions, the endogenous antioxidant system of testis tissue was inhibited at the high doses of cadmium in a short time, resulting in the damage of the testis tissue cells.…”

Section: Discussionmentioning

confidence: 81%

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Sulforaphane Prevents Testicular Damage in Kunming Mice Exposed to Cadmium via Activation of Nrf2/ARE Signaling Pathways

Yang

Long

et al. 2016

IJMS

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Sulforaphane (SFN) is a natural and highly effective antioxidant. Studies suggest that SFN protects cells and tissues against cadmium (Cd) toxicity. This study investigated the protective effect of SFN against oxidative damage in the testes of Kunming mice exposed to cadmium, and explored the possible molecular mechanisms involved. Cadmium greatly reduced the serum testosterone levels in mice, reduced sperm motility, total sperm count, and increased the sperm deformity rate. Cadmium also reduces superoxide dismutase (T-SOD) and glutathione (GSH) levels and increases malondialdehyde (MDA) concentrations. SFN intervention improved sperm quality, serum testosterone, and antioxidant levels. Both mRNA and protein expression of mouse testicular nuclear factor-erythroid 2-related factor 2 (Nrf2) was reduced in cadmium-treated group. Furthermore, the downstream genes of Nrf2, glutathione peroxidase (GSH-Px), γ-glutamyl cysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) were also decreased in cadmium-treated group. SFN intervention increases the expression of these genes. Sulforaphane prevents cadmium-induced testicular damage, probably via activation of Nrf2/ARE signaling.

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Section: Discussionmentioning

confidence: 81%

“…Membranes were incubated with HRP-conjugated secondary antibodies, and chemiluminescence (Super ECL Plus, Applygen, Beijing, China) was analyzed using DNR Bio Imaging Systems and analysis software. Membranes were re-incubated with anti-β-actin (1:2000, Sangon Biotech), for normalization, followed by densitometry [44,47]. …”

Section: Methodsmentioning

confidence: 99%

Sulforaphane Prevents Testicular Damage in Kunming Mice Exposed to Cadmium via Activation of Nrf2/ARE Signaling Pathways

Yang

Long

et al. 2016

IJMS

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“…Previous studies demonstrated that heavy metal‐induced cardiotoxicity is related to oxidative stress 28 . Emerging studies have found that oxidative stress induced by cadmium is associated with increase in the levels of cardiac troponins T and I and cardiac serum markers in Cd‐treated rats 29 . Likewise, As 2 O 3 exposure alters the activity of cardiac enzymes in chicken heart tissues 15 .…”

Section: Discussionmentioning

confidence: 98%

Occupational exposure to manganese and risk of creatine kinase and creatine kinase‐MB elevation among ferromanganese refinery workers

Huang

Liu

et al. 2020

American J Industrial Med

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Background Elevated exposure to manganese (Mn) could induce cardiovascular dysfunction. However, limited research is available on the effects of occupational Mn exposure on myocardial enzymes. We aimed to evaluate the relationships between Mn exposure and myocardial enzyme elevation among Mn‐exposed workers. Methods Data were from a follow‐up investigation of a Mn‐exposed workers healthy cohort in 2017. A total of 744 workers were divided into low‐exposure and high‐exposure groups according to Mn time‐weighted average (Mn‐TWA) of less than or equal to 0.15 mg/m3 or greater than 0.15 mg/m3, respectively. Serum levels of myocardial enzymes, including creatine kinase (CK) and creatine kinase‐MB (CK‐MB), lactic dehydrogenase, α‐hydroxybutyrate dehydrogenase, and aspartate transaminase, were assessed, as well as airborne Mn exposure levels. Results After adjustment for sex, body mass index, seniority, education, current smoking status, current drinking status, and hypertension, Mn‐TWA levels were positively associated with the risk of CK elevation (odds ratio [OR] = 1.47 (95% confidence interval [CI]: 1.18‐1.83) per interquartile range [IQR] increase), and risk of CK‐MB elevation [OR = 1.57 (95% CI: 1.03‐2.38) per IQR increase]. In a stratified analysis, Mn‐TWA levels were positively correlated with CK elevation in workers of seniority greater than 19 years, male workers, current smokers, and drinkers. Conclusion Our results suggest that occupational exposure to Mn is associated with increased risk of CK and CK‐MB elevation. The potential mechanisms of the associations between airborne exposure to Mn and increased risk of these myocardial enzyme elevations warrant further investigation.

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“…In this study, GSP pretreatment (100 mg/kg) reduced Cd-induced disruption of cardiac myofibrils, cardiomyocytes necrosis and apoptosis, production of pro-inflammatory cytokines and increased the levels of anti-oxidant enzymes in rats [172]. Wang et al demonstrated that GSP (195 mg/kg, intragastric administration) treatment prevented deoxycorticosterone (DOCA)-salt-induced cardiovascular remodeling and endothelial dysfunction in mice, in part through the involvement of oxidative stress [173].…”

Section: In Vivo Effects Of Polyphenols Against Oxidative Stress-imentioning

confidence: 99%

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

et al. 2017

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Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes. Polyphenols are a large group of natural compounds ubiquitously expressed in plants, and epidemiological studies have shown associations between a diet rich in polyphenols and the prevention of various ROS-mediated human diseases. Polyphenols reduce cardiomyocytes damage, necrosis, apoptosis, infarct size and improve cardiac function by decreasing oxidative stress-induced production of ROS or RNS. These effects are achieved by the ability of polyphenols to modulate the expression and activity of anti-oxidant enzymes and several signaling pathways involved in cells survival. This report reviews current knowledge on the potential anti-oxidative effects of polyphenols to control the cardiotoxicity induced by ROS and RNS stress.

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RETRACTED: Cadmium induced cardiac oxidative stress in rats and its attenuation by GSP through the activation of Nrf2 signaling pathway

Cited by 56 publications

References 61 publications

Sulforaphane Prevents Testicular Damage in Kunming Mice Exposed to Cadmium via Activation of Nrf2/ARE Signaling Pathways

Sulforaphane Prevents Testicular Damage in Kunming Mice Exposed to Cadmium via Activation of Nrf2/ARE Signaling Pathways

Occupational exposure to manganese and risk of creatine kinase and creatine kinase‐MB elevation among ferromanganese refinery workers

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

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