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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. 3.

Fig. 3

N-acetylation capacity of cultured human hepatocytes in situ towards SMZ (top), ABP (middle) and PABA (bottom). Human hepatocyte samples with NAT2*5B/*5B, NAT2*5B/*6A or NAT2*6A/*6A genotype were incubated with SMZ, ABP or PABA at 10 or 200 μM for 24h. Each bar illustrates mean ± SEM for NAT2*5B/*5B (n=10), NAT2*5B/*6A (n=9), and NAT2*6A/*6A (n=7) individual human hepatocyte samples. Differences in N-acetylation differed significantly as NAT2*5B/*5B > NAT2*5B/*6A > NAT2*6A/*6A towards SMZ at both 10 and 200 μM (p=0.0144 and p= 0.0024) respectively, but not towards ABP (p=0.3548 and p=0.3163) and PABA (p= 0.6631 and p=0.6485) at 10 and 200 μM respectively.