Table 3.

Number and types of H-ras mutations in the livers of male B6C3F1 mice administered 0.14 or 0.70 mmol acrylamide or glycidamide per kg body weight, or the vehicle, intraperitoneally on PNDs 1, 8, and 15

Treatment	H-ras codon 61 mutations	H-ras codon 61 mutation
		CAA → AAA	CAA → CGA	CAA → CTA
Historical controla	235/444b (53%)	139/229 (61%)	68/229 (30%)	22/229 (10%)
Control	1/1 (100%)	0 (0%)	0 (0%)	1 (100%)
0.14 mmol acrylamide per kg body weight	0/2 (0%)	0/2 (0%)	0/2 (0%)	0/2 (0%)
0.70 mmol acrylamide per kg body weight	0/1 (0%)	0/1 (0%)	0/1 (0%)	0/1 (0%)
0.14 mmol glycidamide per kg body weight	0/2 (0%)	0/2 (0%)	0/2 (0%)	0/2 (0%)
0.70 mmol glycidamide per kg body weightc	21/45 (47%)	1/21 (5%)*	14/21 (67%)*	5/21 (24%)*

^aHistorical data for H-ras mutation in hepatocellular adenoma and carcinoma of control B6C3F₁ mice were compiled from literature data.^38-43

^bThe data are expressed as the number of H-ras mutations per number of tumors examined, with the percentage being given in parentheses.

^cIn addition to the H-ras mutations indicated, one CAA → CCA codon 61 mutation and one GGA → GAA codon 12 mutation were detected.

^*The spectrum of codon 61 mutations in the hepatocellular adenoma and carcinoma of B6C3F1 mice administered 0.70 mmol glycidamide per kg body weight was significantly different (p = 0.0001) from the historical control spectrum of H-ras codon 61 mutations, as determined by a hypergeometric test.³⁷