Isoniazid and Rifampicin Produce Hepatic Fibrosis through an Oxidative Stress-Dependent Mechanism

Figure 4

INH and RMP treatment and hepatic oxidative stress. (a) Hepatic GSH and (c) TBAR content in control (white bar) and INH+RMP-treated (black bar) mouse at different weeks. Loss of hepatic GSH content (a) and increased TBAR content (c) in the liver was used as a marker of hepatic oxidative stress. (b) Hepatic CYP2E1 activity in mice. (d) Hepatic NOX activity in mice, for (b) and (d). is the control, and is the INH+RMP-treated mouse; (e) mRNA expression of different isoforms of NOX. Data (a–e) are the of 8 mice per group ( versus vehicle-treated control group; ^# versus INH and RMP-treated mice for 4 weeks; ^‡ versus INH and RMP-treated mice for 4 and 12 weeks in (a)–(d)).

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