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. 2015 Jul 21;90:1351–1367. doi: 10.1007/s00204-015-1561-2

Table 5.

Comparison of apical and transcriptional BMDs in furan-treated males

Pathways Transcriptional BMD(L)s Apical BMD(L)s
# of genes modeled (total # of genes in pathway) BMD median (mg/kg bw) BMDL median (mg/kg bw) Apical endpoints BMD (mg/kg bw) BMDL (mg/kg bw)
Cell damage and apoptosis
p38 MAPK signaling 5 (108) 0.08 0.05 Kupffer cells pigmentation 0.03 0.02
ERK/MAPK signaling 6 (176) 0.17 0.04 Hepatocytes apoptosis 0.03 0.02
NRF2-mediated oxidative stress response 8 (169) 0.62 0.47
Inflammation
LPS/IL-1-mediated inhibition of RXR function 15 (186) 1.1 0.69 ALP 1.49 1.29
Acute phase response signaling 11 (157) 1.22 0.83
Biliary tract damage
Hepatic cholestasis 5 (126) 1.10 0.77 Biliary tract hyperplasia 1.45 0.54
FXR/RXR Activation 6 (79) 1.38  0.91 Biliary tract cholangiofibrosis 1.84 1.02
Bile acid biosynthesis, neutral pathway 2 (10) 1.43 0.94

“# of genes modeled” indicates the number of genes that were significant by ANOVA and could be modeled (i.e., filtered to include genes with BMDs less than the highest dose of 2 mg/kg bw and p value of fit ≥0.1)

“Total # of genes in pathway” indicates all of the genes that are involved in the entire pathway