Her proves that MT is involved the detoxification function of heavy metals. Our investigation showed that the content of MT increased with increasing concentration within the ambient medium and exposure time within 48 h. This R inactivation of the Krt7 gene using gene targeting had been suggests that MT is induced to reduce the level of toxic Cd ions in gill cells via binding to Cd, and to decrease the oxidative damage via scavenging ROS. Although Cd exposure clearly induced MT expression, its synthesis was not proportional to Cd accumulation at a later stage of cadmium exposure, e.g, the Cd accumulation increased but the MT level decreased after 48 h. The Lixisenatide results were consistent with the findings of Ma et al. [23], which demonstrated that MT levels elevated MedChemExpress AN 3199 rapidly to the highest values at 24 h and then declined at 72 h. The data presented hereFigure 3. The effects of Cd on H2O2 content and lipid peroxidation in the gills of S. henanense. (A) H2O2 content; (B) MDA content. The mean expression in each treatment group is shown as a fold increase compared to the mean expression in the control, which had been ascribed an arbitrary value of 1. The values are the means 6 S.D. (n = 3). Asterisks indicate a significant difference to the Inal wing disk (anterior to the left and dorsal to the control (*P,0.05). doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell DeathFigure 4. Histological analysis of Cd-induced gill injury in S. R, this data suggests that Mtap may be acting in a henanense by light microscopy. HE-stained gill section: A : 1006; N: 2006. (A) control; (B) exposure to Group A for 24 h; (C) exposure to Group A for 48 h; (D) exposure to Group A for 72 h; (E) exposure to Group A for 96 h; (F) exposure to Group B for 24 h; (G) exposure to Group B for 48 h; (H) exposure to Group B for 72 h; (I) exposure to Group B for 96 h; (J) exposure to Group C for 24 h; (K) exposure to Group C for 48 h; (L) exposure to Group C for 72 h; (M) exposure to Group C for 96 h; (N) exposure to Group C for 96 h. Co: connection of gill lamellae; EC: epithelium cells; GC: gill cavity; GL: gill lamellae; GA: gill axisx; He: hemocyte. doi:10.1371/journal.pone.0064020.gindicated that oxidative stress and cell damage were more serious after 48 h of exposure because the uptake of Cd exceeded the detoxification capacity of MT. In addition to MT, is the antioxidant defense system keeping the routinely formed ROS at a low non-toxic level [37]. Cd treatment increased GPx and CAT activities before 24 h, respectively, indicating that antioxidant mechanisms are stimulated and can effectively scavenge ROS to maintain a normal cellular balance. The activities of CAT and GPx decreased after 24 h in all treatment groups, suggesting that excessive Cd accumulation resulted in a substantial inhibition of the antioxidant response and the accumulation of oxidative substances. Cd promoted an initialincrease followed by a decrease of SOD. The changes of antioxidant enzyme activities explained changes in the H2O2 level, which had no difference compared with the control at 12 h of the treatment but increased significantly after this period. These results support the MedChemExpress BI-78D3 notion of the “adaptive stage” and the “inhibitive stage”, which proposes that the induction of antioxidant enzymes at the initial exposure time could efficiently attenuate the accumulation of H2O2 and maintain a normal cellular balance, whereas the later inhibitory state renders the enzyme unable to 1676428 sufficiently scavenge the H2O2, leading to oxidative damage [10].Effects of Cd on Oxidative State and Cell DeathFigure 5. TUNEL test of Cd-induced apoptosis in gi.Her proves that MT is involved the detoxification function of heavy metals. Our investigation showed that the content of MT increased with increasing concentration within the ambient medium and exposure time within 48 h. This suggests that MT is induced to reduce the level of toxic Cd ions in gill cells via binding to Cd, and to decrease the oxidative damage via scavenging ROS. Although Cd exposure clearly induced MT expression, its synthesis was not proportional to Cd accumulation at a later stage of cadmium exposure, e.g, the Cd accumulation increased but the MT level decreased after 48 h. The results were consistent with the findings of Ma et al. [23], which demonstrated that MT levels elevated rapidly to the highest values at 24 h and then declined at 72 h. The data presented hereFigure 3. The effects of Cd on H2O2 content and lipid peroxidation in the gills of S. henanense. (A) H2O2 content; (B) MDA content. The mean expression in each treatment group is shown as a fold increase compared to the mean expression in the control, which had been ascribed an arbitrary value of 1. The values are the means 6 S.D. (n = 3). Asterisks indicate a significant difference to the control (*P,0.05). doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell DeathFigure 4. Histological analysis of Cd-induced gill injury in S. henanense by light microscopy. HE-stained gill section: A : 1006; N: 2006. (A) control; (B) exposure to Group A for 24 h; (C) exposure to Group A for 48 h; (D) exposure to Group A for 72 h; (E) exposure to Group A for 96 h; (F) exposure to Group B for 24 h; (G) exposure to Group B for 48 h; (H) exposure to Group B for 72 h; (I) exposure to Group B for 96 h; (J) exposure to Group C for 24 h; (K) exposure to Group C for 48 h; (L) exposure to Group C for 72 h; (M) exposure to Group C for 96 h; (N) exposure to Group C for 96 h. Co: connection of gill lamellae; EC: epithelium cells; GC: gill cavity; GL: gill lamellae; GA: gill axisx; He: hemocyte. doi:10.1371/journal.pone.0064020.gindicated that oxidative stress and cell damage were more serious after 48 h of exposure because the uptake of Cd exceeded the detoxification capacity of MT. In addition to MT, is the antioxidant defense system keeping the routinely formed ROS at a low non-toxic level [37]. Cd treatment increased GPx and CAT activities before 24 h, respectively, indicating that antioxidant mechanisms are stimulated and can effectively scavenge ROS to maintain a normal cellular balance. The activities of CAT and GPx decreased after 24 h in all treatment groups, suggesting that excessive Cd accumulation resulted in a substantial inhibition of the antioxidant response and the accumulation of oxidative substances. Cd promoted an initialincrease followed by a decrease of SOD. The changes of antioxidant enzyme activities explained changes in the H2O2 level, which had no difference compared with the control at 12 h of the treatment but increased significantly after this period. These results support the notion of the “adaptive stage” and the “inhibitive stage”, which proposes that the induction of antioxidant enzymes at the initial exposure time could efficiently attenuate the accumulation of H2O2 and maintain a normal cellular balance, whereas the later inhibitory state renders the enzyme unable to 1676428 sufficiently scavenge the H2O2, leading to oxidative damage [10].Effects of Cd on Oxidative State and Cell DeathFigure 5. TUNEL test of Cd-induced apoptosis in gi.Her proves that MT is involved the detoxification function of heavy metals. Our investigation showed that the content of MT increased with increasing concentration within the ambient medium and exposure time within 48 h. This suggests that MT is induced to reduce the level of toxic Cd ions in gill cells via binding to Cd, and to decrease the oxidative damage via scavenging ROS. Although Cd exposure clearly induced MT expression, its synthesis was not proportional to Cd accumulation at a later stage of cadmium exposure, e.g, the Cd accumulation increased but the MT level decreased after 48 h. The results were consistent with the findings of Ma et al. [23], which demonstrated that MT levels elevated rapidly to the highest values at 24 h and then declined at 72 h. The data presented hereFigure 3. The effects of Cd on H2O2 content and lipid peroxidation in the gills of S. henanense. (A) H2O2 content; (B) MDA content. The mean expression in each treatment group is shown as a fold increase compared to the mean expression in the control, which had been ascribed an arbitrary value of 1. The values are the means 6 S.D. (n = 3). Asterisks indicate a significant difference to the control (*P,0.05). doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell DeathFigure 4. Histological analysis of Cd-induced gill injury in S. henanense by light microscopy. HE-stained gill section: A : 1006; N: 2006. (A) control; (B) exposure to Group A for 24 h; (C) exposure to Group A for 48 h; (D) exposure to Group A for 72 h; (E) exposure to Group A for 96 h; (F) exposure to Group B for 24 h; (G) exposure to Group B for 48 h; (H) exposure to Group B for 72 h; (I) exposure to Group B for 96 h; (J) exposure to Group C for 24 h; (K) exposure to Group C for 48 h; (L) exposure to Group C for 72 h; (M) exposure to Group C for 96 h; (N) exposure to Group C for 96 h. Co: connection of gill lamellae; EC: epithelium cells; GC: gill cavity; GL: gill lamellae; GA: gill axisx; He: hemocyte. doi:10.1371/journal.pone.0064020.gindicated that oxidative stress and cell damage were more serious after 48 h of exposure because the uptake of Cd exceeded the detoxification capacity of MT. In addition to MT, is the antioxidant defense system keeping the routinely formed ROS at a low non-toxic level [37]. Cd treatment increased GPx and CAT activities before 24 h, respectively, indicating that antioxidant mechanisms are stimulated and can effectively scavenge ROS to maintain a normal cellular balance. The activities of CAT and GPx decreased after 24 h in all treatment groups, suggesting that excessive Cd accumulation resulted in a substantial inhibition of the antioxidant response and the accumulation of oxidative substances. Cd promoted an initialincrease followed by a decrease of SOD. The changes of antioxidant enzyme activities explained changes in the H2O2 level, which had no difference compared with the control at 12 h of the treatment but increased significantly after this period. These results support the notion of the “adaptive stage” and the “inhibitive stage”, which proposes that the induction of antioxidant enzymes at the initial exposure time could efficiently attenuate the accumulation of H2O2 and maintain a normal cellular balance, whereas the later inhibitory state renders the enzyme unable to 1676428 sufficiently scavenge the H2O2, leading to oxidative damage [10].Effects of Cd on Oxidative State and Cell DeathFigure 5. TUNEL test of Cd-induced apoptosis in gi.Her proves that MT is involved the detoxification function of heavy metals. Our investigation showed that the content of MT increased with increasing concentration within the ambient medium and exposure time within 48 h. This suggests that MT is induced to reduce the level of toxic Cd ions in gill cells via binding to Cd, and to decrease the oxidative damage via scavenging ROS. Although Cd exposure clearly induced MT expression, its synthesis was not proportional to Cd accumulation at a later stage of cadmium exposure, e.g, the Cd accumulation increased but the MT level decreased after 48 h. The results were consistent with the findings of Ma et al. [23], which demonstrated that MT levels elevated rapidly to the highest values at 24 h and then declined at 72 h. The data presented hereFigure 3. The effects of Cd on H2O2 content and lipid peroxidation in the gills of S. henanense. (A) H2O2 content; (B) MDA content. The mean expression in each treatment group is shown as a fold increase compared to the mean expression in the control, which had been ascribed an arbitrary value of 1. The values are the means 6 S.D. (n = 3). Asterisks indicate a significant difference to the control (*P,0.05). doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell DeathFigure 4. Histological analysis of Cd-induced gill injury in S. henanense by light microscopy. HE-stained gill section: A : 1006; N: 2006. (A) control; (B) exposure to Group A for 24 h; (C) exposure to Group A for 48 h; (D) exposure to Group A for 72 h; (E) exposure to Group A for 96 h; (F) exposure to Group B for 24 h; (G) exposure to Group B for 48 h; (H) exposure to Group B for 72 h; (I) exposure to Group B for 96 h; (J) exposure to Group C for 24 h; (K) exposure to Group C for 48 h; (L) exposure to Group C for 72 h; (M) exposure to Group C for 96 h; (N) exposure to Group C for 96 h. Co: connection of gill lamellae; EC: epithelium cells; GC: gill cavity; GL: gill lamellae; GA: gill axisx; He: hemocyte. doi:10.1371/journal.pone.0064020.gindicated that oxidative stress and cell damage were more serious after 48 h of exposure because the uptake of Cd exceeded the detoxification capacity of MT. In addition to MT, is the antioxidant defense system keeping the routinely formed ROS at a low non-toxic level [37]. Cd treatment increased GPx and CAT activities before 24 h, respectively, indicating that antioxidant mechanisms are stimulated and can effectively scavenge ROS to maintain a normal cellular balance. The activities of CAT and GPx decreased after 24 h in all treatment groups, suggesting that excessive Cd accumulation resulted in a substantial inhibition of the antioxidant response and the accumulation of oxidative substances. Cd promoted an initialincrease followed by a decrease of SOD. The changes of antioxidant enzyme activities explained changes in the H2O2 level, which had no difference compared with the control at 12 h of the treatment but increased significantly after this period. These results support the notion of the “adaptive stage” and the “inhibitive stage”, which proposes that the induction of antioxidant enzymes at the initial exposure time could efficiently attenuate the accumulation of H2O2 and maintain a normal cellular balance, whereas the later inhibitory state renders the enzyme unable to 1676428 sufficiently scavenge the H2O2, leading to oxidative damage [10].Effects of Cd on Oxidative State and Cell DeathFigure 5. TUNEL test of Cd-induced apoptosis in gi.Her proves that MT is involved the detoxification function of heavy metals. Our investigation showed that the content of MT increased with increasing concentration within the ambient medium and exposure time within 48 h. This suggests that MT is induced to reduce the level of toxic Cd ions in gill cells via binding to Cd, and to decrease the oxidative damage via scavenging ROS. Although Cd exposure clearly induced MT expression, its synthesis was not proportional to Cd accumulation at a later stage of cadmium exposure, e.g, the Cd accumulation increased but the MT level decreased after 48 h. The results were consistent with the findings of Ma et al. [23], which demonstrated that MT levels elevated rapidly to the highest values at 24 h and then declined at 72 h. The data presented hereFigure 3. The effects of Cd on H2O2 content and lipid peroxidation in the gills of S. henanense. (A) H2O2 content; (B) MDA content. The mean expression in each treatment group is shown as a fold increase compared to the mean expression in the control, which had been ascribed an arbitrary value of 1. The values are the means 6 S.D. (n = 3). Asterisks indicate a significant difference to the control (*P,0.05). doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell DeathFigure 4. Histological analysis of Cd-induced gill injury in S. henanense by light microscopy. HE-stained gill section: A : 1006; N: 2006. (A) control; (B) exposure to Group A for 24 h; (C) exposure to Group A for 48 h; (D) exposure to Group A for 72 h; (E) exposure to Group A for 96 h; (F) exposure to Group B for 24 h; (G) exposure to Group B for 48 h; (H) exposure to Group B for 72 h; (I) exposure to Group B for 96 h; (J) exposure to Group C for 24 h; (K) exposure to Group C for 48 h; (L) exposure to Group C for 72 h; (M) exposure to Group C for 96 h; (N) exposure to Group C for 96 h. Co: connection of gill lamellae; EC: epithelium cells; GC: gill cavity; GL: gill lamellae; GA: gill axisx; He: hemocyte. doi:10.1371/journal.pone.0064020.gindicated that oxidative stress and cell damage were more serious after 48 h of exposure because the uptake of Cd exceeded the detoxification capacity of MT. In addition to MT, is the antioxidant defense system keeping the routinely formed ROS at a low non-toxic level [37]. Cd treatment increased GPx and CAT activities before 24 h, respectively, indicating that antioxidant mechanisms are stimulated and can effectively scavenge ROS to maintain a normal cellular balance. The activities of CAT and GPx decreased after 24 h in all treatment groups, suggesting that excessive Cd accumulation resulted in a substantial inhibition of the antioxidant response and the accumulation of oxidative substances. Cd promoted an initialincrease followed by a decrease of SOD. The changes of antioxidant enzyme activities explained changes in the H2O2 level, which had no difference compared with the control at 12 h of the treatment but increased significantly after this period. These results support the notion of the “adaptive stage” and the “inhibitive stage”, which proposes that the induction of antioxidant enzymes at the initial exposure time could efficiently attenuate the accumulation of H2O2 and maintain a normal cellular balance, whereas the later inhibitory state renders the enzyme unable to 1676428 sufficiently scavenge the H2O2, leading to oxidative damage [10].Effects of Cd on Oxidative State and Cell DeathFigure 5. TUNEL test of Cd-induced apoptosis in gi.Her proves that MT is involved the detoxification function of heavy metals. Our investigation showed that the content of MT increased with increasing concentration within the ambient medium and exposure time within 48 h. This suggests that MT is induced to reduce the level of toxic Cd ions in gill cells via binding to Cd, and to decrease the oxidative damage via scavenging ROS. Although Cd exposure clearly induced MT expression, its synthesis was not proportional to Cd accumulation at a later stage of cadmium exposure, e.g, the Cd accumulation increased but the MT level decreased after 48 h. The results were consistent with the findings of Ma et al. [23], which demonstrated that MT levels elevated rapidly to the highest values at 24 h and then declined at 72 h. The data presented hereFigure 3. The effects of Cd on H2O2 content and lipid peroxidation in the gills of S. henanense. (A) H2O2 content; (B) MDA content. The mean expression in each treatment group is shown as a fold increase compared to the mean expression in the control, which had been ascribed an arbitrary value of 1. The values are the means 6 S.D. (n = 3). Asterisks indicate a significant difference to the control (*P,0.05). doi:10.1371/journal.pone.0064020.gEffects of Cd on Oxidative State and Cell DeathFigure 4. Histological analysis of Cd-induced gill injury in S. henanense by light microscopy. HE-stained gill section: A : 1006; N: 2006. (A) control; (B) exposure to Group A for 24 h; (C) exposure to Group A for 48 h; (D) exposure to Group A for 72 h; (E) exposure to Group A for 96 h; (F) exposure to Group B for 24 h; (G) exposure to Group B for 48 h; (H) exposure to Group B for 72 h; (I) exposure to Group B for 96 h; (J) exposure to Group C for 24 h; (K) exposure to Group C for 48 h; (L) exposure to Group C for 72 h; (M) exposure to Group C for 96 h; (N) exposure to Group C for 96 h. Co: connection of gill lamellae; EC: epithelium cells; GC: gill cavity; GL: gill lamellae; GA: gill axisx; He: hemocyte. doi:10.1371/journal.pone.0064020.gindicated that oxidative stress and cell damage were more serious after 48 h of exposure because the uptake of Cd exceeded the detoxification capacity of MT. In addition to MT, is the antioxidant defense system keeping the routinely formed ROS at a low non-toxic level [37]. Cd treatment increased GPx and CAT activities before 24 h, respectively, indicating that antioxidant mechanisms are stimulated and can effectively scavenge ROS to maintain a normal cellular balance. The activities of CAT and GPx decreased after 24 h in all treatment groups, suggesting that excessive Cd accumulation resulted in a substantial inhibition of the antioxidant response and the accumulation of oxidative substances. Cd promoted an initialincrease followed by a decrease of SOD. The changes of antioxidant enzyme activities explained changes in the H2O2 level, which had no difference compared with the control at 12 h of the treatment but increased significantly after this period. These results support the notion of the “adaptive stage” and the “inhibitive stage”, which proposes that the induction of antioxidant enzymes at the initial exposure time could efficiently attenuate the accumulation of H2O2 and maintain a normal cellular balance, whereas the later inhibitory state renders the enzyme unable to 1676428 sufficiently scavenge the H2O2, leading to oxidative damage [10].Effects of Cd on Oxidative State and Cell DeathFigure 5. TUNEL test of Cd-induced apoptosis in gi.
