“…Nonetheless, the BrdU-LIs show that the CDAA diet caused an enhanced and high degree of cell proliferation in females that increased steadily for 12 (28), there appears to be no consensus as yet about their nature and role in lipotrope-deficient diet models (9,14,16,31,35). The major uncertainties stem from the fact that in the latter, enzyme-altered hepatocytes develop in small numbers, like those with which &dquo;spontaneous&dquo; foci have been observed to emerge in colony or control groups of rats (31,35 of developed foci of GST-P-positive hepatocytes (24,36). These findings led to the proposal (15, 24) that 8-OHG may play an important role in the initiation stage of hepatocarcinogenesis by lipotrope-deficient diets, given that this adduct is mutagenic (2,10,21,22), and that specific pathways exist for its removal (3,7,8,18,20), which could be overwhelmed or deteriorated by the high rate of compensatory mitogenesis induced by these diets in the liver of male rats (14,16 …”