Lls of S. henanense. Stained gill section 2006. (A) control; (B) Group

Lls of S. henanense. Stained gill section 2006. (A) control; (B) Group A; (C) Group B; (D) Group C. The apoptotic cellular nucleus was brown (circle), non-apoptotic cellular nucleus was blue. doi:10.1371/journal.pone.0064020.gCadmium is known to induce ROS, thereby causing lipid peroxidation [24,38]. Long-term exposure to Cd disrupts the equilibrium between ROS generation and detoxification. Thus,ROS are generated following acute Cd intoxication and play important roles in tissue damage [39]. MDA levels are commonly accepted as an effective biomarker of toxic pollutant exposure [10]. In the present study, H2O2 levels increased significantly at 24 h which MedChemExpress 34540-22-2 correlated with the decrease in antioxidant enzyme activities. A lack of increase in MDA content before 24 h may indicate negligible tissue damages caused by oxidative radicals, which might be due to the protective effects of the antioxidant system and MT. With the constitutive increase of an Cd-induced H2O2 content, a general trend for the induction of MDA can be observed. Low basal enzyme activity after 24 h treatment appeared to impair the ability of scavenging free radicals in animals and, in turn, resulted in elevated MDA levels. The MDA level increase was followed by consistent decreases in antioxidant enzyme activities. Based on these observations, we can infer that 16985061 a variation in membrane damage may represent different toxicities exhibited by different exposure durations. The longer the exposure time, the more severe are cells subjected to oxidative stress and damage. Oxidative stress provides a threat to cells. H2O2 activates the apoptotic response at the beginning of peroxide exposure, whereas inhibition of apoptosis leads to necrosis when the apoptotic process can be inhibited [21]. It was reported that Cd caused an intracellular stable accumulation of peroxide oxidation and death by apoptosis in U-937 cells, and pre-incubation with BSO, a GSHdepleting agent, switched the mode of death from apoptosis toFigure 6. Effects of Cd on subcellular structure of S. henanense gills. A : control. (A) normal epithelial cell with nucleus and a large number of cytoplasmic organelles; (B) normal hemocyte in the gill cavity. C : exposure to Group C for 48 h. (C) cytoplasm of epithelial cell with the vacuolar enlargement (black triangle) and organelles reduction; (D) nucleus of epithelial cell with chromatin condensation and extremely irregular nuclear membrane; (E) purchase Eliglustat hemocytes in the gill cavity with apoptotic characteristic. F : exposure to Group C for 96 h. (F) cytoplasm of degenerative and necrotic epithelial cells with scare organelles and broken membrane (asterisks); (G) nucleus of necrotic epithelial cells with nuclear membrane collapses (asterisks); (H) hemocytes in the gill cavity with inflammatory response. A: 60006; B: 80006; C: 80006; D: 100006; E: 100006; F: 80006; G: 80006; H: 50006. N: nucleus; LG: large granules; SG: small granules; GC: gill cavity. doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell Deathnecrosis in Cd-treated cells [16]. So a modulation of antioxidant defense systems in cells affects form and intensity of cell death [40]. Cell death resulting from Cd intoxication has been confirmed to induce both necrosis and apoptosis. The ratio between both types of cell death is dose- and cell-type-dependent [41]. Our previous study showed that Cd induced an apoptotic response in gill cells of freshwater crab depending on the H2O2 production [25]. Bu.Lls of S. henanense. Stained gill section 2006. (A) control; (B) Group A; (C) Group B; (D) Group C. The apoptotic cellular nucleus was brown (circle), non-apoptotic cellular nucleus was blue. doi:10.1371/journal.pone.0064020.gCadmium is known to induce ROS, thereby causing lipid peroxidation [24,38]. Long-term exposure to Cd disrupts the equilibrium between ROS generation and detoxification. Thus,ROS are generated following acute Cd intoxication and play important roles in tissue damage [39]. MDA levels are commonly accepted as an effective biomarker of toxic pollutant exposure [10]. In the present study, H2O2 levels increased significantly at 24 h which correlated with the decrease in antioxidant enzyme activities. A lack of increase in MDA content before 24 h may indicate negligible tissue damages caused by oxidative radicals, which might be due to the protective effects of the antioxidant system and MT. With the constitutive increase of an Cd-induced H2O2 content, a general trend for the induction of MDA can be observed. Low basal enzyme activity after 24 h treatment appeared to impair the ability of scavenging free radicals in animals and, in turn, resulted in elevated MDA levels. The MDA level increase was followed by consistent decreases in antioxidant enzyme activities. Based on these observations, we can infer that 16985061 a variation in membrane damage may represent different toxicities exhibited by different exposure durations. The longer the exposure time, the more severe are cells subjected to oxidative stress and damage. Oxidative stress provides a threat to cells. H2O2 activates the apoptotic response at the beginning of peroxide exposure, whereas inhibition of apoptosis leads to necrosis when the apoptotic process can be inhibited [21]. It was reported that Cd caused an intracellular stable accumulation of peroxide oxidation and death by apoptosis in U-937 cells, and pre-incubation with BSO, a GSHdepleting agent, switched the mode of death from apoptosis toFigure 6. Effects of Cd on subcellular structure of S. henanense gills. A : control. (A) normal epithelial cell with nucleus and a large number of cytoplasmic organelles; (B) normal hemocyte in the gill cavity. C : exposure to Group C for 48 h. (C) cytoplasm of epithelial cell with the vacuolar enlargement (black triangle) and organelles reduction; (D) nucleus of epithelial cell with chromatin condensation and extremely irregular nuclear membrane; (E) hemocytes in the gill cavity with apoptotic characteristic. F : exposure to Group C for 96 h. (F) cytoplasm of degenerative and necrotic epithelial cells with scare organelles and broken membrane (asterisks); (G) nucleus of necrotic epithelial cells with nuclear membrane collapses (asterisks); (H) hemocytes in the gill cavity with inflammatory response. A: 60006; B: 80006; C: 80006; D: 100006; E: 100006; F: 80006; G: 80006; H: 50006. N: nucleus; LG: large granules; SG: small granules; GC: gill cavity. doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell Deathnecrosis in Cd-treated cells [16]. So a modulation of antioxidant defense systems in cells affects form and intensity of cell death [40]. Cell death resulting from Cd intoxication has been confirmed to induce both necrosis and apoptosis. The ratio between both types of cell death is dose- and cell-type-dependent [41]. Our previous study showed that Cd induced an apoptotic response in gill cells of freshwater crab depending on the H2O2 production [25]. Bu.

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