Absence of B0AT1 attenuated aristolochic acid (AA)-induced markers of senescence and inflammation in the kidney cortex. Kidney mRNA expression of p21 (A), Lcn2 [neutrophil gelatinase-associated lipocalin (NGAL); B], and C-C motif chemokine ligand 2 [Ccl2; monocyte chemoattractant protein-1 (MCP-1)] and C-C motif chemokine receptor 2 (Ccr2) (C) in mice treated with vehicle or AA. mRNA expression was normalized to the ribosomal protein L19 (Rpl19) gene. Values are means ± SE and dots show individual mouse data. Two-way ANOVA was performed to probe for a significant effect of treatment (PAA), genotypes (PSlc6a19), or the interaction between the two factors (Pinter). If the interaction was statistically significant, then a pair-wise multiple comparison procedure (Holm–Sidak method) identified the significant effects. *P < 0.05 vs. wild-type (WT) mice; #P < 0.05 vs. vehicle. n = 6–14 mice/group.