Potential mechanism of cadmium-induced cytotoxicity in rat hepatocytes: inhibitory action of cadmium on mitochondrial respiratory activity

Koizumi, Toshiaki; Yokota, Tetsuo; Shirakura, Hiroaki; Hideki, Tatsumoto; Suzuki, Kazuo

doi:10.1016/0300-483x(94)90171-6

Cited by 51 publications

(17 citation statements)

References 23 publications

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“…As soon as in 1971, Mustafa and Cross reported Cd-induced effects on electron and energy transfer reactions in the mitochondria of pulmonary alveolar macrophages. More recent studies confirmed the general view of mitochondria as one of the primary cellular targets of metals such as Cd (Müller 1986) and discussed potential mechanisms of Cd-induced cytotoxicity (Cameron et al 1986;Early et al 1992;Koizumi et al 1994;Al-Nasser 2000;Tang and Shaikh 2001;Belyaeva et al 2002Belyaeva et al , 2004Belyaeva et al , 2008Belyaeva and Korotkov 2003;Lee et al 2004;Pathak and Khandelwal 2006). More specifically, Belyaeva et al (2006) found that Cd-induced effects in AS-30D rat ascites hepatoma cells, manifested by cell necrosis and/or apoptosis, involve ROS generation.…”

Section: Mitochondrial Ros Productionmentioning

confidence: 76%

“…The antioxidative defense system, for example, is activated via Nfr2 binding to antioxidant responsive elements (Chen et al 2008). Some researchers suggest a direct involvement of Cd, as HO-1 (heme oxygenase 1) and HSP70 are shown to be regulated via Cd-and metal-responsive elements (CdRE/MRE) (Koizumi et al 1994(Koizumi et al , 2007.…”

Section: Cadmium: An Oxidative Challengementioning

confidence: 99%

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Cadmium stress: an oxidative challenge

et al. 2010

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At the cellular level, cadmium (Cd) induces both damaging and repair processes in which the cellular redox status plays a crucial role. Being not redox-active, Cd is unable to generate reactive oxygen species (ROS) directly, but Cd-induced oxidative stress is a common phenomenon observed in multiple studies. The current review gives an overview on Cd-induced ROS production and anti-oxidative defense in organisms under different Cd regimes. Moreover, the Cd-induced oxidative challenge is discussed with a focus on damage and signaling as downstream responses. Gathering these data, it was clear that oxidative stress related responses are affected during Cd stress, but the apparent discrepancies observed in between the different studies points towards the necessity to increase our knowledge on the spatial and temporal ROS signature under Cd stress. This information is essential in order to reveal the exact role of Cd-induced oxidative stress in the modulation of downstream responses under a diverse array of conditions.

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Section: Mitochondrial Ros Productionmentioning

confidence: 76%

Section: Cadmium: An Oxidative Challengementioning

confidence: 99%

Cadmium stress: an oxidative challenge

et al. 2010

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“…Mitochondria are considered critical cellular targets in cadmium hepatotoxicity and are the most sensitive organelles in the toxic effects of the metal (Muller and Ohnesorge 1984;Koizumi et al 1994Koizumi et al , 1996Casalino et al 1997;Esteve et al 1999). Impairment of mitochondrial function and subsequent reduction of oxidative metabolism are also key events in inducing apoptosis (Esteve et al 1999).…”

Section: Discussionmentioning

confidence: 98%

The hepatoprotective effect of putrescine against cadmium-induced acute liver injury

Tzirogiannis¹,

Panoutsopoulos²,

Demonakou

et al. 2004

Archives of Toxicology

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The hepatoprotective effect of putrescine against cadmium liver injury was investigated. Male Wistar rats were injected with a dose of cadmium (6.5 mg CdCl(2)/kg bodyweight, intraperitoneally). Normal saline (group I) or putrescine (300 micro mol/kg bodyweight; group II) were injected 2, 5 and 8 h later. A number of animals of both groups were killed 0, 12, 16, 24, 48 or 60 h after cadmium intoxication. Liver tissue was histologically assessed for necrosis, apoptosis, peliosis, mitoses, and inflammatory infiltration. Apoptosis was also quantified by the TUNEL assay for hepatocytes and nonparenchymal liver cells. The discrimination between hepatic cell subpopulations was achieved histochemically. The mitotic index in hematoxylin-eosin-stained sections and by the immunochemical detection of Ki67 nuclear antigen, (3)H-thymidine incorporation into hepatic DNA, and hepatic thymidine kinase activity were all used as indices of liver regeneration. Both hepatocyte apoptosis and liver necrosis evolved in a biphasic temporal pattern. Nonparenchymal cell apoptosis and peliosis hepatis evolved in a monophasic pattern and were correlated closely. Putrescine administration totally reversed liver necrosis and hepatocyte apoptosis. The time profile of nonparenchymal apoptosis was altered and peliosis hepatis was also totally attenuated. In conclusion, putrescine protected hepatocytes and modulated the mechanism of cadmium-induced acute hepatotoxicity.

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“…For example, when P. japonicus were exposed to different concentrations of heavy metals, the following could be observed: an increased number of nephrocytes in gill filaments; a blackened appearance of the gills; necrosis of gill cells resulting in narrowed or obstructed hemolymphatic vessels; the appearance of a space between the cuticle and the epithelial cells, which contain black electron-dense material; and even fragmentation of nuclei within gill cells. Thus, the main pathological effect on the respiratory system caused by cadmium is the interference with the respiratory system, including cellular respiration (Koizumi et al 1994;Spicer and Weber 1991).…”

Section: Discussionmentioning

confidence: 99%

Effects of zinc and cadmium on oxygen consumption and ammonium excretion in pink shrimp (Farfantepenaeus paulensis, Pérez-Farfante, 1967, Crustacea)

Barbieri

2008

Ecotoxicology

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In Brazil, pink shrimp (Farfantepenaeus paulensis) is an important commercially exploited species and is an ideal animal for studying the impairment caused by the effects of heavy metals that are often detected in coastal areas. The main purpose of the present study was to detect the acute toxicity of cadmium and zinc to F. paulensis and investigate their effects on oxygen consumption and ammonium excretion, investigations that have not been carried out in this species before. First, the acute toxicity of zinc and cadmium to F. paulensis for 24, 48, 72, and 96 h--medium lethal concentration was examined, which resulted in the following values: 9.39, 6.00, 4.88, and 3.31 mg/l for zinc and 2.35, 1.67, 1.26, and 0.83 mg/l for cadmium. Furthermore, we also found that exposure of shrimp to zinc and cadmium caused an inhibition in oxygen consumption of 25 and 32.4%, respectively, relative to the control. In addition, after separate exposure to cadmium and zinc, elevations in ammonium excretion were obtained, which were 42.85 and 51.85% higher than the control, respectively.

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Potential mechanism of cadmium-induced cytotoxicity in rat hepatocytes: inhibitory action of cadmium on mitochondrial respiratory activity

Cited by 51 publications

References 23 publications

Cadmium stress: an oxidative challenge

Cadmium stress: an oxidative challenge

The hepatoprotective effect of putrescine against cadmium-induced acute liver injury

Effects of zinc and cadmium on oxygen consumption and ammonium excretion in pink shrimp (Farfantepenaeus paulensis, Pérez-Farfante, 1967, Crustacea)

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