Abstract |
The microsomal metabolites and mutagenic activity of four cyclopenta-fused benz(a)anthracenes; benz(j)aceanthrylene (B(j)A), benz(e)aceanthrylene (B(e)A), benz(l)aceanthrylene (B(l)A) and benz(k)acephenanthrylene (B(k)A) have been studied. Arocolor-1254 induced rat liver microsomes metabolized B(j)A to: B(j)A-1,2-dihydrodiol, B(j)A-9,10-dihydrodiol, B(j)A-11,12-dihydrodiol and 10-hydroxy-B(j)A; B(e)A to: B(e)A-1,2-dihydrodiol, B(e)A-3,4-dihydrodiol, and B(e)A-5,6-dihydrodial; B(l)A to: B(l)A-1,2-dihydrodiol, B(l)A-4,5-dihydrodiol and B(l)A-7,8-dihydrodiol; and B(k)A to B(k)A-4,5-dihydrodiol and B(k)A-89-dihydrodiol. With each PAH, metabolism occurred on the cyclopentaring. All four isomers were active as gene mutagens in S. typhimurium and in Chinese hamster V79 cells. In the S. typhimurium mutation studies using Aroclor-1254 induced rat liver S9, B(j)A, B(e)A, and B(l)A required significantly less microsomal protein for maximal mutation response than B(k)A and B(a)P suggesting a one-step activation mechanism, presumably on the cyclopenta-fused ring. B(j)A, B(e)A, and B(l)A were significantly more mutagenic than B(k)A and B(a)P in S. typhimurium. |