Long-term cadmium exposure accelerates age-related mitochondrial changes in renal epithelial cells

Takaki, Aya; Jimi, Shiro; Segawa, Masaru; Hisano, Satoshi; Takebayashi, Shigeo; Iwasaki, Hiroshi

doi:10.1016/j.tox.2004.06.005

Cited by 42 publications

(17 citation statements)

References 43 publications

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“…It has been found that Cd produces various pathological conditions, including hepatic and renal dysfunctions, testicular damage, and respiratory and nervous system disorders (13, 14, 16,17). Cd induced chronic toxicity has been shown as histological and ultrastructural by various investigators in experiments using various species of animals (18,19). During acute exposure, Cd-induced necrosis and cellular damage are produced in the kidney, liver and testicular tissue; chronic exposure results in damage to the kidney, pancreas, and bone (20).…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Quercetin Against Renal Toxicity Induced by Cadmium in Rats

Aktoz¹

2012

Balkan Med J

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Objective: The aim of the present study was to examine the protective effect of quercetine (QE) against cadmium (Cd)-induced renal toxicity. Material and Methods:A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated and Cd-treated with QE; each group containing 8 animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in the QE treated groups were given QE (15 mg/kg body weight) once a day intraperitoneally starting 2 days prior to Cd injection during the study period.Results: The renal histology in Cd-treated rats showed mesangial expansion, thickening of capsular basement membranes, glomerular basement membranes and tubular basement membranes, characterized by an increase in periodic acid Schiff (PAS)-positive areas as compared with control animals. With the QE treatment, despite the presence of only a few swollen glomeruli, we noticed a marked protection of renal structure when compared with the Cd-treated rats. Furthermore, QE pretreatment resulted in increased proliferating cell nuclear antigen (PCNA) immunoreactivity and decreased the activity of Terminal Transferase dUTP Nick End Labeling (TUNEL). Conclusion:These findings suggest that QE may attenuate Cd-induced renal toxicity.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Quercetin Against Renal Toxicity Induced by Cadmium in Rats

Aktoz¹

2012

Balkan Med J

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“…Growing evidence indicates that Cd exposure leads to mitochondrial loss in liver cells, reflected by a decrease in both mitochondrial DNA copy number and in the expression of components of the mitochondrial respiratory chain. [8][9][10][11][12] However, the mechanism by which Cd induces mitochondrial loss during Cd-induced hepatotoxicity is not fully understood. Identifying the mechanism that underlies Cd-induced mitochondrial reduction during hepatotoxicity is an important area of clinical research, and the present results offer insight into new mitochondrial targets for therapeutic intervention in Cd-affected populations.…”

Section: Introductionmentioning

confidence: 99%

Dynamin 1-like-dependent mitochondrial fission initiates overactive mitophagy in the hepatotoxicity of cadmium

Zhang

et al. 2013

Autophagy

129

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“…Cadmium (Cd) is not an essential metal for animals but its essentiality has been suggested for marine diatoms (Lane and Morel, 2000). Cd has long been known to be toxic; itai-itai disease which developed in Japan, is the most severe form of chronic Cd poisoning caused by prolonged oral Cd ingestion ( Takaki et al, 2004). Levels of As in aquatic organisms vary over a wide range of concentrations and chemical forms.…”

Section: Introductionmentioning

confidence: 99%

Arsenic and cadmium in the marine macroalgae (Porphyra yezoensis and Laminaria Japonica) — forms and concentrations

Zhao

Shang

Ning

et al. 2012

Chemical Speciation & Bioavailability

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Total arsenic, inorganic arsenic (iAs), total cadmium concentrations and chemical forms of cadmium were analysed in Porphyra yezoensis collected monthly from January to April in 2011 and in Laminaria Japonica collected monthly from March to July in 2010. Results showed that total As concentrations in P. yezoensis were much lower than those in L. Japonica. The iAs concentrations in both macroalgae were all below the maximum limit according to the legislation in China, while total Cd concentrations in all samples of P. yezoensis exceeded the maximum limit. The percentage of iAs to total As decreased in both macroalgae with the time. The results provide important information showing that both macroalgae are able to metabolise inorganic arsenic to organic forms. Thus both macroalgae have evolved arsenic resistance which is linked to the capability of metabolising toxic inorganic arsenic. In addition, the results suggest that the transformation rate of arsenate to organic arsenic in both algae increases with the growth and metabolic rate that increase with elevated environmental temperature. Temperatures rise from January to April in Jiangsu province and from March to July in Liaoning Province. Most Cd was associated with pectates and protein (extractable by 1 M NaCl) in both algae, and only a small percentage of the Cd was inorganic (extractable by 80% ethanol). The Cd chemical forms have no obvious relationship with the time in both algae.

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Long-term cadmium exposure accelerates age-related mitochondrial changes in renal epithelial cells

Cited by 42 publications

References 43 publications

Protective Effect of Quercetin Against Renal Toxicity Induced by Cadmium in Rats

Protective Effect of Quercetin Against Renal Toxicity Induced by Cadmium in Rats

Dynamin 1-like-dependent mitochondrial fission initiates overactive mitophagy in the hepatotoxicity of cadmium

Arsenic and cadmium in the marine macroalgae (Porphyra yezoensis and Laminaria Japonica) — forms and concentrations

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