<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dostalek M</submitter><funding>NIDDK NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>17147-57</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2427356</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>283(25)</volume><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., </pubmed_abstract><journal>The Journal of biological chemistry</journal><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.</pubmed_title><pmcid>PMC2427356</pmcid><funding_grant_id>P50 GM16431</funding_grant_id><funding_grant_id>R01 ES007462-13</funding_grant_id><funding_grant_id>R01 DK48831</funding_grant_id><funding_grant_id>P01 ES13125</funding_grant_id><funding_grant_id>P30 ES000267</funding_grant_id><funding_grant_id>R01 ES007462</funding_grant_id><funding_grant_id>R01 ES08089</funding_grant_id><funding_grant_id>R01 ES10042</funding_grant_id><funding_grant_id>R37 CA090426</funding_grant_id><funding_grant_id>R01 ES07462</funding_grant_id><pubmed_authors>Ding X</pubmed_authors><pubmed_authors>Martin MV</pubmed_authors><pubmed_authors>Dostalek M</pubmed_authors><pubmed_authors>Hardy KD</pubmed_authors><pubmed_authors>Morrow JD</pubmed_authors><pubmed_authors>Gu J</pubmed_authors><pubmed_authors>Johnson JA</pubmed_authors><pubmed_authors>Gonzalez FJ</pubmed_authors><pubmed_authors>Chen C</pubmed_authors><pubmed_authors>Johnson DA</pubmed_authors><pubmed_authors>Guengerich FP</pubmed_authors><pubmed_authors>Milne GL</pubmed_authors></additional><is_claimable>false</is_claimable><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.</name><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., </description><dates><release>2008-01-01T00:00:00Z</release><publication>2008 Jun</publication><modification>2025-05-29T21:52:18.826Z</modification><creation>2025-05-29T21:52:18.826Z</creation></dates><accession>S-EPMC2427356</accession><cross_references><pubmed>18442974</pubmed><doi>10.1074/jbc.M802447200</doi><doi>10.1074/jbc.m802447200</doi></cross_references></HashMap>