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• W2103764145 abstract "To identify novel factors or mechanisms that are important for the resistance of tissues to chemical toxicity, we have determined the mechanisms underlying the previously observed increases in resistance to acetaminophen (APAP) toxicity in the lateral nasal gland (LNG) of the male <i>Cyp2g1</i>-null/<i>Cyp2a5</i>-low mouse. Initial studies established that <i>Cyp2a5</i>-null mice, but not a newly generated strain of <i>Cyp2g1</i>-null mice, were resistant to APAP toxicity in the LNG; therefore, subsequent studies were focused on the <i>Cyp2a5</i>-null mice. Compared with the wild-type (WT) male mouse, the <i>Cyp2a5</i>-null male mouse had intact capability to metabolize APAP to reactive intermediates in the LNG, as well as unaltered circulating levels of APAP, APAP-GSH, APAP-glucuronide, and APAP-sulfate. However, it displayed reduced tissue levels of APAP and APAP-GSH and increased tissue levels of testosterone and salivary androgen-binding protein (ABP) in the LNG. Furthermore, we found that ABP was able to compete with GSH and cellular proteins for adduction with reactive metabolites of APAP in vitro. The amounts of APAP-ABP adducts formed in vivo were greater, whereas the amounts of APAP adducts formed with other cellular proteins were substantially lower, in the LNG of APAP-treated male <i>Cyp2a5</i>-null mice compared with the LNG of APAP-treated male WT mice. We propose that through its critical role in testosterone metabolism, CYP2A5 regulates 1) the bioavailability of APAP and APAP-GSH (presumably through modulation of the rates of xenobiotic excretion from the LNG) and 2) the expression of ABP, which can quench reactive APAP metabolites and thereby spare critical cellular proteins from inactivation." @default.
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• W2103764145 date "2011-01-20" @default.
• W2103764145 modified "2023-09-25" @default.
• W2103764145 title "A Novel Defensive Mechanism against Acetaminophen Toxicity in the Mouse Lateral Nasal Gland: Role of CYP2A5-Mediated Regulation of Testosterone Homeostasis and Salivary Androgen-Binding Protein Expression" @default.
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• W2103764145 doi "https://doi.org/10.1124/mol.110.070045" @default.
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