Cadmium induces reactive oxygen species generation and lipid peroxidation in cortical neurons in culture

López, Esther; Arce, Carmen; Oset-Gasque, María Jesús; Cañadas, S.; González, M.P.

doi:10.1016/j.freeradbiomed.2005.10.062

Cited by 357 publications

(225 citation statements)

References 54 publications

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“…Numerous studies suggest that metals induce oxidative stress in a variety of cell types (Ercal et al 2001;Valko et al 2005). For example, cadmium is a nonredox metal that has been shown to induce oxidative stress by increasing ROS indirectly in S. cerevisiae and neurons (Brennan and Schiestl 1996;López et al 2006;Cuypers et al 2010). These previous studies provided a potential link between Rho1 and Ycf1, but also raised some important questions.…”

mentioning

confidence: 99%

The Rho1 GTPase Acts Together With a Vacuolar Glutathione S-Conjugate Transporter to Protect Yeast Cells From Oxidative Stress

Lee

Singh²,

Snider

et al. 2011

Genetics

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Maintenance of redox homeostasis is critical for the survival of all aerobic organisms. In the budding yeast Saccharomyces cerevisiae, as in other eukaryotes, reactive oxygen species (ROS) are generated during metabolism and upon exposure to environmental stresses. The abnormal production of ROS triggers defense mechanisms to avoid the deleterious consequence of ROS accumulation. Here, we show that the Rho1 GTPase is necessary to confer resistance to oxidants in budding yeast. Temperature-sensitive rho1 mutants (rho1 ts ) are hypersensitive to oxidants and exhibit high accumulation of ROS even at a semipermissive temperature. Rho1 associates with Ycf1, a vacuolar glutathione S-conjugate transporter, which is important for heavy metal detoxification in yeast. Rho1 and Ycf1 exhibit a two-hybrid interaction with each other and form a bimolecular fluorescent complex on the vacuolar membrane. A fluorescent-based complementation assay suggests that the GTP-bound Rho1 associates with Ycf1 and that their interaction is enhanced upon exposure to hydrogen peroxide. The rho1 ts mutants also exhibit hypersensitivity to cadmium, while cells carrying a deletion of YCF1 or mutations in a component of the Pkc1-MAP kinase pathway exhibit little or minor sensitivity to oxidants. We thus propose that Rho1 protects yeast cells from oxidative stress by regulating multiple downstream targets including Ycf1. Since both Rho1 and Ycf1 belong to highly conserved families of proteins, similar mechanisms may exist in other eukaryotes.

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mentioning

confidence: 99%

The Rho1 GTPase Acts Together With a Vacuolar Glutathione S-Conjugate Transporter to Protect Yeast Cells From Oxidative Stress

Lee

Singh²,

Snider

et al. 2011

Genetics

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“…Cadmium induced neuronal toxicity is also due to induction of ROS leading to oxidative stress (Lopez et al, 2006;Chen et al, 2008Chen et al, , 2011Thevenod et al, 2009 Mitogen-activated protein kinases (MAPKs) are important signal transduction enzymes that are involved in many cellular processes including development, differentiation, proliferation and apoptosis (Hamanoue et al, 2007;Vacotto et al, 2008). Studies have demonstrated that ERK, NK and p38 MAPK, play a critical role in cadmium induced apoptosis of many cell types including neuronal cells Nemmiche et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Lin¹,

Peng²,

Yang³

et al. 2015

Bangladesh J Pharmacol

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Cadmium, a toxic environmental contaminant, induces oxidative stress leading to various neurodegenerative disorders, where it interferes with homeos-tasis of intracellular free calcium ([Ca2+]i), leading to cellular damage and apoptosis. We investigated whether resveratrol, a plant-derived antioxidant could offer protection against cadmium-induced neuroapoptosis. Primary cortical neurons were exposed to cadmium (10 or 20 µM) with/without prior exposure to resveratrol (5, 10 or 20 µM) for 12 hours and unexposed cells served as control. Resveratrol caused marked reduction in cadmium-induced neuronal apoptosis and down-regulated caspase-3 expressions. Cadmium-induced marked elevations in reactive oxygen species, and ([Ca2+]i) levels were potentially reduced by resveratrol. Resveratrol effectively regulated the alterations observed in the activation levels of mitogen-activated protein kinases (MAPKs) and proteins of mammalian target of rapamycin (mTOR) pathways. Thus, resveratrol effectively protected the cortical neurons exposed to cadmium by modulating the ([Ca2+]i) levels and regulating the MAPK/mTOR pathways.

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“…Significant Cd-induced increases in the levels of malondialdehyde (MDA) and protein carbonyl have been reported in cell cultures and animals exposed to Cd (Lopez et al 2006;Donpunha et al 2011). …”

Section: Cadmium-induced Cardiovascular Dysfunctionmentioning

confidence: 99%

Oxidative Stress and Cardiovascular Dysfunction Associated with Cadmium Exposure: Beneficial Effects of Curcumin and Tetrahydrocurcumin

Kukongviriyapan

Apaijit

Kukongviriyapan

2016

Tohoku J. Exp. Med.

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Cadmium (Cd) is a non-essential heavy metal with high toxicity potential. Humans are exposed to Cd present in diet, polluted air, and cigarette smoke. Cd exposure has been associated with increased risk of chronic diseases, including hypertension, atherosclerosis, diabetes, and nephropathy, all of which could be attributable to dysfunctional endothelial and smooth muscle cells. Cd toxicity is correlated with increased reactive oxygen formation and depletion of antioxidants, resulting in an oxidative stress. Chelation of Cd has proved useful in the removal of the Cd burden. However, several chelating agents cause side effects in clinical usage. Recent studies have shown that the antioxidant compounds curcumin and tetrahydrocurcumin can alleviate vascular dysfunction and high blood pressure caused by Cd toxicity. In chronic Cd exposure, these antioxidants protect vascular endothelium by increasing nitric oxide (NO•) bioavailability and improving vascular function. Antioxidant activity against Cd intoxication results directly and/or indirectly through free radical scavenging, metal chelation, enhanced expression of the antioxidant defense system, regulation of inflammatory enzymes, increase in NO• bioavailability, and reduction of gastrointestinal absorption and tissue Cd accumulation. This review summarizes current knowledge of Cd-induced oxidative stress and cardiovascular dysfunction and a possible protective effect conferred by the antioxidants curcumin and tetrahydrocurcumin.

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Cadmium induces reactive oxygen species generation and lipid peroxidation in cortical neurons in culture

Cited by 357 publications

References 54 publications

The Rho1 GTPase Acts Together With a Vacuolar Glutathione S-Conjugate Transporter to Protect Yeast Cells From Oxidative Stress

The Rho1 GTPase Acts Together With a Vacuolar Glutathione S-Conjugate Transporter to Protect Yeast Cells From Oxidative Stress

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Oxidative Stress and Cardiovascular Dysfunction Associated with Cadmium Exposure: Beneficial Effects of Curcumin and Tetrahydrocurcumin

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