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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: Arch Toxicol. 2017 May 17;91(7):2655–2661. doi: 10.1007/s00204-017-1988-8

Fig. 4.

Fig. 4

N-acetylation capacity of cultured human hepatocytes in situ towards SMZ (top), ABP (middle) and PABA (bottom). Human hepatocyte samples with NAT2*4/*5B or NAT2*4/*6A genotype were incubated with SMZ, ABP or PABA at 10 or 200 μM for 24h. Each bar illustrates mean ± SEM for NAT2*4/*5B (n=8) or NAT2*4/*6A (n=9) individual human hepatocyte samples. N-acetylation capacity did not differ significantly between samples with NAT2*4/*5B or NAT2*4/*6A genotype at 10 or 200 μM for SMZ (p=0.7547 and p= 0.5399) ABP (p=0.3096 and p=0.6534) or PABA (p= 0.6536 and p=0.8199) respectively.