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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

Toxicology (Amsterdam), 2004-10, Vol.203 (1), p.145-154 [Periódico revisado por pares]

Shannon: Elsevier Ireland Ltd

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Título:
Long-term cadmium exposure accelerates age-related mitochondrial changes in renal epithelial cells
Autor: Takaki, Aya ; Jimi, Shiro ; Segawa, Masaru ; Hisano, Satoshi ; Takebayashi, Shigeo ; Iwasaki, Hiroshi
Assuntos: Adenosine Triphosphate - metabolism ; Aging - drug effects ; Animals ; Biological and medical sciences ; Cadmium Poisoning - pathology ; Chemical and industrial products toxicology. Toxic occupational diseases ; Chronic cadmium intoxication ; DNA, Mitochondrial - biosynthesis ; DNA, Mitochondrial - metabolism ; Electron Transport Complex IV - metabolism ; Epithelial Cells - drug effects ; Epithelial Cells - pathology ; Female ; Immunohistochemistry ; Itai-Itai disease ; Kidney Cortex - drug effects ; Kidney Cortex - metabolism ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - metabolism ; Medical sciences ; Metals and various inorganic compounds ; Mitochondria - drug effects ; Mitochondria - pathology ; Mitochondrial DNA deletion ; Oxidation-Reduction ; Phosphatidylcholines - metabolism ; Proximal tubule ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Toxicology
É parte de: Toxicology (Amsterdam), 2004-10, Vol.203 (1), p.145-154
Notas: ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
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Descrição: Long-term cadmium exposure leads to mitochondrial dysfunction in the proximal tubular epithelial cells. Mitochondrial DNA deletion may contribute to the pathogenesis of cadmium-induced nephropathy. The aim of our study is to clarify the accumulation of mitochondrial DNA deletion and mitochondrial dysfunction in the renal cortex of rats injected three times/week with 1 ml of 1 mM CdCl 2 or saline for 80 weeks. After 40-week cadmium injection, mitochondrial number diminished, and cadmium in the renal cortex reached a saturation level. At this time interval, nearly 30% of cadmium in the whole cell fraction was found in the mitochondria. Cytochrome c oxidase (COX) activity in the proximal tubular epithelial cells decreased after 40-week exposure of cadmium. Oxidized phosphatidylcholine (oxPC) started to accumulate in the cytochrome c-positive mitochondria in some tubular epithelial cells after 80-week exposure. After 40 weeks, accumulation of the 4834-bp deletion in mitochondrial DNA was evident in both control and cadmium-treated groups. However, the amount of accumulated mitochondrial DNA deletion tended to increase after 40-week exposure, and was significantly greater after 80 weeks of exposure, compared to the control. Our results indicate that long-term cadmium exposure in rats accelerates accumulation of 4834-bp mitochondrial DNA deletions and impairment of mitochondrial function associated with accumulation of oxidized product.
Editor: Shannon: Elsevier Ireland Ltd
Idioma: Inglês

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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

Shannon: Elsevier Ireland Ltd

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