{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dostalek M"],"funding":["NIDDK NIH HHS","NIEHS NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["17147-57"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2427356"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["283(25)"],"pubmed_abstract":["Reactive oxygen species (ROS) and oxidative stress have been considered in a variety of disease models, and cytochrome P450 (P450) enzymes have been suggested to be a source of ROS. Induction of P450s by phenobarbital (PB), beta-naphthoflavone (betaNF), or clofibrate in a mouse model increased ROS parameters in the isolated liver microsomes, but isoniazid treatment did not. However, when F(2)-isoprostanes (F(2)-IsoPs) were measured in tissues and urine, PB showed the strongest effect and betaNF had a measurable but weaker effect. The same trend was seen when an Nfr2-based transgene reporter sensitive to ROS was analyzed in the mice. This pattern had been seen earlier with F(2)-IsoPs both in vitro and in vivo with rats (Dostalek, M., Brooks, J. D., Hardy, K. D., Milne, G. L., Moore, M. M., "],"journal":["The Journal of biological chemistry"],"pubmed_title":["Development of oxidative stress by cytochrome P450 induction in rodents is selective for barbiturates and related to loss of pyridine nucleotide-dependent protective systems."],"pmcid":["PMC2427356"],"funding_grant_id":["P50 GM16431","R01 ES007462-13","R01 DK48831","P01 ES13125","P30 ES000267","R01 ES007462","R01 ES08089","R01 ES10042","R37 CA090426","R01 ES07462"],"pubmed_authors":["Ding X","Martin MV","Dostalek M","Hardy KD","Morrow JD","Gu J","Johnson JA","Gonzalez FJ","Chen C","Johnson DA","Guengerich FP","Milne GL"],"additional_accession":[]},"is_claimable":false,"name":"Development of oxidative stress by cytochrome P450 induction in rodents is selective for barbiturates and related to loss of pyridine nucleotide-dependent protective systems.","description":"Reactive oxygen species (ROS) and oxidative stress have been considered in a variety of disease models, and cytochrome P450 (P450) enzymes have been suggested to be a source of ROS. Induction of P450s by phenobarbital (PB), beta-naphthoflavone (betaNF), or clofibrate in a mouse model increased ROS parameters in the isolated liver microsomes, but isoniazid treatment did not. However, when F(2)-isoprostanes (F(2)-IsoPs) were measured in tissues and urine, PB showed the strongest effect and betaNF had a measurable but weaker effect. The same trend was seen when an Nfr2-based transgene reporter sensitive to ROS was analyzed in the mice. This pattern had been seen earlier with F(2)-IsoPs both in vitro and in vivo with rats (Dostalek, M., Brooks, J. D., Hardy, K. D., Milne, G. L., Moore, M. M., ","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Jun","modification":"2025-05-29T21:52:18.826Z","creation":"2025-05-29T21:52:18.826Z"},"accession":"S-EPMC2427356","cross_references":{"pubmed":["18442974"],"doi":["10.1074/jbc.M802447200","10.1074/jbc.m802447200"]}}