Table 2.
CYP2A6*35 is associated with lower in vivo CYP2A6 activity.
| Population | Genotype | n | Mean adjusted 3HC/COT | S.D. | p-value | % of wildtype activity |
|---|---|---|---|---|---|---|
| African Canadian | *1/*1 | 151 | 1.20 | 0.63 | 100 | |
| *1/*35 | 10 | 0.84 | 0.50 | 0.02 | 70 | |
| *9/*35a | 1 | 0.47 | - | 39 | ||
| *17/*35a | 3 | 0.08 | 0.14 | 7 | ||
| African American | *1/*1 | 258 | 1.21 | 0.80 | 100 | |
| *1/*35 | 20 | 0.75 | 0.26 | 0.003b | 62 | |
| *35/*35a | 1 | 0.51 | - | 42 | ||
| *9/*35a | 2 | 0.78 | 0.51 | 62 | ||
| *17/*35a | 3 | 0.27 | 0.09 | 22 |
n=number of samples, S.D. = standard deviation.
the number of individuals with greater than one variant was too small for statistical analyses.
the p-value obtained does not include the homozygote CYP2A6*35 individual. The ratio was derived from plasma metabolite levels following oral nicotine intake or ad libitum smoking among the African Canadian and African American population, respectively. The effect of CYP2A6*35 remained significant in both populations when the wildtype group included individuals with at least one CYP2A6*1B allele (i.e. CYP2A6*1A/*1B and CYP2A6*1B/*1B). The 3H/COT ratios among individuals with CYP2A6*35 compared to individuals with only CYP2A6*1B were as follows: 0.84±0.50 vs. 1.25±0.66, p=0.03 among African Canadians and 0.75±0.26 vs. 1.38±0.75, p<0.001 among African Americans. The p-values are from the regression model as described in the methods section with the dependent variable being log 3HC/COT, controlling for gender and smoking. When the data was analyzed with a Mann-Whitney test where the dependent variable was 3HC/COT (i.e. not log normalized), and where the effects of gender and smoking were not considered, the effect of CYP2A6*35 remained significant in both populations (African Canadian p=0.016 and the African American p=0.001).