Effect of cadmium-induced oxidative stress on antioxidative enzymes in mitochondria and cytoplasm of CRL-1439 rat liver cells

Abstract

Cadmium affects human health through occupational and environmental exposure. In this report, we present the response of mitochondrial and cytoplasmic antioxidant enzymes of CRL-1439 cells exposed to different concentrations (0-150 μM) of CdCl 2 for 24 h at 37˚C. Exposure of liver cells to 50 μM CdCl 2 increased mitochondrial catalase and glutathione reductase (GR) activities more than the cytoplasmic enzymes. Although the mitochondrial selenium-dependent glutathione peroxidase (Se-GPx) showed less enzymatic activity than the cytoplasmic enzyme, the mitochondrial selenium-independent glutathione peroxidase (non-Se-GPx) showed a slight increase in activity over its cytoplasmic counterpart compared to untreated controls. With 100 μM CdCl 2 , catalase maintained an increase in specific activity in mitochondria over the cytoplasmic enzyme compared to the controls. The level of GR was higher in the cytoplasm than in the mitochondria. However, the activity of Se-GPx and non-Se-GPx decreased slightly in the mitochondria compared to their cytoplasmic counterparts. Exposure of cells to 150 μM CdCl 2 decreased all antioxidant enzyme activities compared to the 100 μM CdCl 2-treated samples due to toxic effect. Each antioxidant enzyme exhibited its own pattern of activation or inhibition upon exposure to different concentrations of cadmium, with more oxidative stress observed in the mitochondria.

Impact of cadmium on the level of hepatic metallothioneins, essential elements, and selected enzymes in the experimental rat model

“…Localization of enzymes may play an important role, too. The in vitro experiments showed increased mitochondrial catalase and glutathione reductase (GR) activities more than the cytoplasmic enzymes (Latinwo et al 2006). Cd is bound to erythrocytes or albumin during blood transport and subsequently is deposited into different tissues.…”

Cadmium-Induced Pathologies: Where Is the Oxidative Balance Lost (or Not)?

“…In these cells, more oxidative stress was observed in mitochondria rather than in cytoplasm and depending on different concentrations of Cd (0–150 μM CdCl 2 for 24 h), antioxidant enzymes were activated or inhibited. A CAT assay was performed separately on mitochondrial (mit) and cytoplasmic (cyt) extracts of Cd-treated cells, which showed an increased mit-CAT activity of 60.3%, 88.0%, and 80% to 50, 100 and 150 μM of CdCl 2 respectively while an increase in cyt-CAT activity was restricted to 10.4% and 50.5% at 50 and 100 μM CdCl 2 [48]. A further increase in dose to 150 μM CdCl 2 decreased the cyt-CAT activity to the untreated control levels.…”

“…The cyt-GR activity was the highest at 100 μM CdCl 2 . It appears that mitochondrial enzymes were more effective in reducing various ROS than their cytoplasmic counterparts and the activities of antioxidant enzymes in the cytoplasm were not as high as the mitochondrial enzymes upon Cd treatments [48]. Although the mitochondrial antioxidant system is very effective, Cd-induced ROS production in mitochondria is strongly associated with cell death.…”

Assessing the Quality of Household and Drinking Water in Tongi Industrial Zone of Bangladesh and Its Toxicological Impact on Healthy Sprague Dawley Rats

“…The co-exposure of metal/ metalloid mixtures of heavy metals in household and drinking water produce severe effects at both relatively high and low dose levels [31,[41][42][43][44][45][46]. This study is a brief reflection of the toxicological effects of industrialization on water resources, as well as the pharmacological effects of contaminated household and drinking water on animal model of an industrialized area in a developing country.…”