Higher in the Cd group and the Ro4402257 web administration of DMS to Cd-exposed rats leads to a decrease in DCF, protein carbonyl, and MDA levels. The data represent means ?standard error of the mean (SEM).Figure 2 Cu, Zn-Superoxide dismutase 1 (SOD1), catalase (CAT), and glutathione peroxidase (GPx) activity in the hippocampi of control, DMS-, Cd-, Cd-DMS-treated rats. * Indicates a significant difference between the control and Cd groups (P <0.05); # indicates a significant difference between the Cd and Cd/DMS groups (P <0.05; n = 7 per group). Antioxidant enzyme activities are order R1503 significantly lower in the Cd group and the administration of DMS to Cd-exposed rats ameliorates the reduction of enzyme activities. The effect on GPx activity is greater than that on SOD1 or CAT activities. The data represent means ?standard error of the mean (SEM).significantly decreased TSH content and increased protein carbonylation in the hippocampus. This result confirmed those of previous studies, which showed that CdKim et al. BMC Complementary and Alternative Medicine 2014, 14:428 http://www.biomedcentral.com/1472-6882/14/Page 6 ofFigure 3 Total sulfhydryl groups (TSH), reduced glutathione (GSH), glutathione reductase (GR), and glutathione-S-transferase (GST) in the hippocampi of control, DMS-, Cd-, Cd/DMS-treated rats. * Indicates a significant difference between the control and Cd groups (P <0.05); # indicates a significant difference between the Cd and Cd/DMS groups (P <0.05; n = 5 per group). GR activity, TSH levels, and GSH levels are significantly increased after exposure to Cd, while GST activity is significantly increased. The administration of DMS to Cd-exposed rats ameliorates or reverses the changes of enzyme activities or levels. The data represent means ?standard error of the mean (SEM).administration significantly increased ROS-mediated reactions in the brain, including the hippocampus [30], and kidney [31]. We PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26024392 also estimated lipid peroxidation by measuring MDA level, which is a major oxidation product of peroxidized polyunsaturated fatty acids [32]. Repeated administration of Cd significantly increased MDA levels in the hippocampus. This result is consistent with previous studies showing that exposure to Cd for 30 days significantly increases MDA levels in hippocampal tissue [33,34]. However, supplementation with DMS significantly reduced MDA levels in the hippocampus. This suggests that DMS potently inhibits Cd-induced lipid peroxidation in the hippocampus. This result is in accordance with a recent study showing that rutin isolated from Dendropanax morbifera L eille significantly decreases rotenone-induced generation of reactive oxygen species in SH-SY5Y cells [14]. In this study, we also determined the effects of DMS and/or Cd on the activity of SOD1, CAT, and GPx in the hippocampus because Cd has been shown to inhibit antioxidant enzymes [33-38]. We found that Cd exposure for 4 weeks significantly reduced the activities of SOD1, CAT, and GPx in the hippocampus. These data are in agreement with those of previous studies showing that GPx, SOD1, Mn-SOD, and CAT activities in thehippocampus are significantly decreased after Cd exposure for 30 days [33,34]. Cd attacks intracellular sulfhydryl groups and disrupts organelles [39], because most antioxidant enzymes become inactive when Cd binds to their active sites [40]. Supplementation with DMS prevented the Cd-induced inhibition of SOD1, CAT, and GPx activities in the hippocampus, suggesting that the a.Higher in the Cd group and the administration of DMS to Cd-exposed rats leads to a decrease in DCF, protein carbonyl, and MDA levels. The data represent means ?standard error of the mean (SEM).Figure 2 Cu, Zn-Superoxide dismutase 1 (SOD1), catalase (CAT), and glutathione peroxidase (GPx) activity in the hippocampi of control, DMS-, Cd-, Cd-DMS-treated rats. * Indicates a significant difference between the control and Cd groups (P <0.05); # indicates a significant difference between the Cd and Cd/DMS groups (P <0.05; n = 7 per group). Antioxidant enzyme activities are significantly lower in the Cd group and the administration of DMS to Cd-exposed rats ameliorates the reduction of enzyme activities. The effect on GPx activity is greater than that on SOD1 or CAT activities. The data represent means ?standard error of the mean (SEM).significantly decreased TSH content and increased protein carbonylation in the hippocampus. This result confirmed those of previous studies, which showed that CdKim et al. BMC Complementary and Alternative Medicine 2014, 14:428 http://www.biomedcentral.com/1472-6882/14/Page 6 ofFigure 3 Total sulfhydryl groups (TSH), reduced glutathione (GSH), glutathione reductase (GR), and glutathione-S-transferase (GST) in the hippocampi of control, DMS-, Cd-, Cd/DMS-treated rats. * Indicates a significant difference between the control and Cd groups (P <0.05); # indicates a significant difference between the Cd and Cd/DMS groups (P <0.05; n = 5 per group). GR activity, TSH levels, and GSH levels are significantly increased after exposure to Cd, while GST activity is significantly increased. The administration of DMS to Cd-exposed rats ameliorates or reverses the changes of enzyme activities or levels. The data represent means ?standard error of the mean (SEM).administration significantly increased ROS-mediated reactions in the brain, including the hippocampus [30], and kidney [31]. We PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26024392 also estimated lipid peroxidation by measuring MDA level, which is a major oxidation product of peroxidized polyunsaturated fatty acids [32]. Repeated administration of Cd significantly increased MDA levels in the hippocampus. This result is consistent with previous studies showing that exposure to Cd for 30 days significantly increases MDA levels in hippocampal tissue [33,34]. However, supplementation with DMS significantly reduced MDA levels in the hippocampus. This suggests that DMS potently inhibits Cd-induced lipid peroxidation in the hippocampus. This result is in accordance with a recent study showing that rutin isolated from Dendropanax morbifera L eille significantly decreases rotenone-induced generation of reactive oxygen species in SH-SY5Y cells [14]. In this study, we also determined the effects of DMS and/or Cd on the activity of SOD1, CAT, and GPx in the hippocampus because Cd has been shown to inhibit antioxidant enzymes [33-38]. We found that Cd exposure for 4 weeks significantly reduced the activities of SOD1, CAT, and GPx in the hippocampus. These data are in agreement with those of previous studies showing that GPx, SOD1, Mn-SOD, and CAT activities in thehippocampus are significantly decreased after Cd exposure for 30 days [33,34]. Cd attacks intracellular sulfhydryl groups and disrupts organelles [39], because most antioxidant enzymes become inactive when Cd binds to their active sites [40]. Supplementation with DMS prevented the Cd-induced inhibition of SOD1, CAT, and GPx activities in the hippocampus, suggesting that the a.
