Glutathione and mitochondria determine acute defense responses and adaptive processes in cadmium-induced oxidative stress and toxicity of the kidney

Nair, Ambily Ravindran; Lee, Wing-Kee; Smeets, Karen; Swennen, Quirine; Sanchez, Amparo Yovanna Castro; Totzke, Frank; Cuypers, Ann

doi:10.1007/s00204-014-1401-9

Cited by 91 publications

(54 citation statements)

References 47 publications

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“…It was demonstrated that NOS played a critical role on the Cd-induced ROS generation [22]. Cd 2+ also damages mitochondria which results in a disturbance of respiratory activity, alteration of inner membrane permeability, loss of membrane potential, swelling, activation of caspases and apoptosis, induction of mtDNA mutations and alteration of gene expression, as well as the induction of ROS [23]. Various studies connect Cd with oxidative stress, since this metal can alter the antioxidant defense system and caused marked disturbances of the antioxidant defense system both in vivo and in vitro [24].…”

Section: Discussionmentioning

confidence: 99%

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

Xia

Luo

Liu

et al. 2015

Biol Trace Elem Res

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Molybdenum (Mo) is an essential element for human beings and animals; however, high dietary intake of Mo can lead to adverse reactions. Cadmium (Cd) is harmful to health. To investigate the toxicity of Mo combined with Cd in duck kidneys, 240 ducks were randomly divided into six groups and treated with a commercial diet containing Mo, Cd or Mo combined with Cd. Kidneys were collected on days 30, 60, 90 and 120 for determining the expression of heat shock proteins (HSPs), including HSP60, HSP70 and HSP90 in the kidney through quantitative RT-PCR. We also determined the antioxidant activity indexes in the kidney mitochondria. Moreover, kidney tissues at 120 days were subjected to histopathological analysis with the optical microscope. The results indicated that the expression of HSPs was highly significantly (P <0.01) upregulated in the kidneys of the combination groups and the Cd group. Exposure to Cd and a high dose of Mo decreased the total antioxidative capacity and the activity of xanthine oxidase, while malondialdehyde levels and the activity of nitric oxide synthase increased compared with those of the control groups in the kidney mitochondria. This was particularly evident at 90 and 120 days. Histopathological lesions included congestion and bleeding in the renal interstitium, swelling of the distal convoluted tubule epithelial cells, granular degeneration and blister degeneration in the renal tubular epithelial cells. These results suggest that a combination of Mo and Cd leads to greater tissue damage and has a synergistic effect on kidney damage. Oxidative damage of kidney mitochondria may be a potential nephrotoxicity mechanism of molybdenum and cadmium, and the high expression of HSPs may play a role in the resistance of kidney toxicity induced by Mo and Cd.

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Section: Discussionmentioning

confidence: 99%

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

Xia

Luo

Liu

et al. 2015

Biol Trace Elem Res

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“…By virtue of its small molecular weight, Cd-MT complexes pass through the glomeruli into the glomerular filtrate and are reabsorbed by PTCs and are subjected to degradation. Presumably, degradation of Cd-MT complexes results in a release of unbound or free Cd 2+ ions, causing oxidative stress and depletion of endogenous anti-oxidants such as glutathione and bilirubin (Nair et al 2015). Cd-induced oxidative stress produces damage to a variety of proteins in tubular epithelial cells, notably the Na/K-ATPase (Thevenod and Friedmann 1999).…”

Section: Cadmium and The Pathogenesis Of Hypertension In Humansmentioning

confidence: 99%

Kidney Cadmium Toxicity, Diabetes and High Blood Pressure: The Perfect Storm

Satarug

Vesey

Gobé

2017

Tohoku J. Exp. Med.

102

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“…Evidence from animal studies suggests an important factor of lipid peroxidation and degradation of phospholipids in kidney damage is caused by Pb toxicity, which leads to a loss of membrane integrity [4]. Besides, when cells are overwhelmed by oxidative stress, genes involved in cell death signaling are activated to induce apoptosis or necrosis to remove irreversibly damaged cells [5]. Therefore, an increase in the level of apoptosis may underline the pathogenesis of kidney injury.…”

Section: Introductionmentioning

confidence: 99%

GSPE reduces lead-induced oxidative stress by activating the Nrf2 pathway and suppressing miR153 and GSK-3β in rat kidney

et al. 2017

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Lead (Pb) is a global environmental health hazard that leads to nephrotoxicity. However, the effective treatment of Pb-induced nephrotoxicity remains elusive. Grape seed procyanidin extract (GSPE) has beneficial properties for multiple biological functions. Therefore, the present study investigated whether GSPE reduced Pb-induced nephrotoxicity as well as the protective mechanism of GSPE in a well-established 35-day Pb induced nephrotoxicity rat model. The results showed that GSPE normalized Pb-induced oxidative stress, histological damage, inflammatory, apoptosis, and changes of miR153 and glycogen synthase kinase 3β (GSK-3β) levels in rat kidney. Moreover, GSPE enhanced the induction of phase II detoxifying enzymes (heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1) by increasing nuclear factor-erythroid-2-related factor 2 (Nrf2) expression. This study identifies for the first time that Pb-induced oxidative stress in rat kidney is attenuated by GSPE treatment via activating Nrf2 signaling pathway and suppressing miR153 and GSK-3β. Nrf2 signaling provides a new therapeutic target for renal injury induced by Pb, and GSPE could be a potential natural agent to protect against Pb-induced nephrotoxicity.

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Glutathione and mitochondria determine acute defense responses and adaptive processes in cadmium-induced oxidative stress and toxicity of the kidney

Cited by 91 publications

References 47 publications

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

Kidney Cadmium Toxicity, Diabetes and High Blood Pressure: The Perfect Storm

GSPE reduces lead-induced oxidative stress by activating the Nrf2 pathway and suppressing miR153 and GSK-3β in rat kidney

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