PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2890191-1 1987 The administration of nickel to rats resulted in a dose-dependent increase in the level of hepatic glutathione and in the activities of glutathione reductase and glutathione-S-transferase with a concomitant decrease in the activities of glutathione peroxidase and gamma-glutamyl transpeptidase. Nickel 22-28 hematopoietic prostaglandin D synthase Rattus norvegicus 162-187 8103437-2 1993 The acute combined effects of cadmium (Cd) and nickel (Ni) on rat hepatic glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB) and ethacrynic acid (EAA) were determined and compared to those of Cd or Ni alone. Nickel 47-53 hematopoietic prostaglandin D synthase Rattus norvegicus 74-99 8103437-2 1993 The acute combined effects of cadmium (Cd) and nickel (Ni) on rat hepatic glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB) and ethacrynic acid (EAA) were determined and compared to those of Cd or Ni alone. Nickel 47-53 hematopoietic prostaglandin D synthase Rattus norvegicus 101-104 1977209-4 1990 In the liver, nickel effects included increased LPO (by 30%), decreased CAT and GSH-Px activities (both by 15%), decreased GSH level (by 33%), decreased GSSG-R activity (by 10%) and decreased GST activity (by 35%); SOD, GGT, copper, and iron remained unchanged. Nickel 14-20 hematopoietic prostaglandin D synthase Rattus norvegicus 192-195 10602394-3 1999 Administration of nickel (250 micromol Ni/kg body wt) to female Wistar rats, resulted in increase in the reduced glutathione (GSH) content [kidney (*P<0.05) and liver (**P<0.001)] and Glutathione-S-transferase (GST) and glutathione reductase (GR) activities [kidney and liver, (**P<0.001)]. Nickel 18-24 hematopoietic prostaglandin D synthase Rattus norvegicus 190-215 20950607-5 2011 The toxic effect of nickel was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase and non-enzymatic antioxidants like reduced glutathione, total sulfhydryl groups, vitamin C and vitamin E levels were significantly decreased. Nickel 20-26 hematopoietic prostaglandin D synthase Rattus norvegicus 171-196 20021064-6 2005 However, nickel treatment to normal rats caused a significant increase in the activity of enzymes catalase and GST and in the levels of LPO, whereas the levels of GSH get significantly depressed. Nickel 9-15 hematopoietic prostaglandin D synthase Rattus norvegicus 111-114 15535990-5 2004 Nickel treatment to the normal control animals, resulted in a significant increase in lipid peroxidation and enzyme activities of catalase and glutathione-S-transferase. Nickel 0-6 hematopoietic prostaglandin D synthase Rattus norvegicus 143-168 15535990-8 2004 Interestingly, when Zn was supplemented to nickel treated rats, the activities of catalase, and glutathione-S-transferase and the levels of GSH and lipid peroxidation came back to within normal limits. Nickel 43-49 hematopoietic prostaglandin D synthase Rattus norvegicus 96-121 10602394-3 1999 Administration of nickel (250 micromol Ni/kg body wt) to female Wistar rats, resulted in increase in the reduced glutathione (GSH) content [kidney (*P<0.05) and liver (**P<0.001)] and Glutathione-S-transferase (GST) and glutathione reductase (GR) activities [kidney and liver, (**P<0.001)]. Nickel 18-24 hematopoietic prostaglandin D synthase Rattus norvegicus 217-220