Regular ArticleAcetaminophen Nephrotoxicity in the CD-1 Mouse. II. Protection by Probenecid and AT-125 without Diminution of Renal Covalent Binding
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Probenecid prevents acute tubular necrosis in a mouse model of aristolochic acid nephropathy
2012, Kidney InternationalCitation Excerpt :AA (5 mg/kg body weight) or PEG was injected once a day and PBN (150 mg/kg body weight) twice a day. These dosing regimens of PBN have been shown to inhibit OAT.20 Plasma creatinine (PCr) level, TI lesions, DNA-repair processes (proliferating cell nuclear antigen tissue expression), and AA-DNA adduct formation were quantified in each group after 2, 4, 5, and 8 days of AA injections.
Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity in CD-1 mice: I. Enhancement of acetaminophen nephrotoxicity by acetaminophen-cysteine
2005, Toxicology and Applied PharmacologyCitation Excerpt :Reactive thiol cleavage products of haloalkene thioethers, such as 1,2-dichlorovinyl-l-cysteine, are also implicated in the generation of DNA damage leading to mutagenicity (Dekant and Henschler, 1999). However, a role for the renal β-lyase pathway in APAP nephrotoxicity is unlikely because the β-lyase inhibitor (aminooxy)acetic (AOAA) acid did not modulate acetaminophen nephrotoxicity in our CD-1 mouse model (Emeigh Hart et al., 1996). The nephrotoxicity of quinone GSH conjugates results from their electrophilic nature and their ability to undergo redox cycling (Bolton et al., 2000).
Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity II. Possible involvement of the γ-glutamyl cycle
2005, Toxicology and Applied Pharmacology