Abstract
Intraperitoneal administration of 6.5 mg of in vitro methylated DNA (meDNA) containing 1.5 x 10(-4) mM of O6-methylguanine (6MG) to male outbred rats weighing 150 g led to a considerable decrease in the activity of liver O6-alkylguanine-DNA alkyltransferase (AT). One hour after treatment there occurred a 4- to 5-fold decrease in the AT activity followed by its slow recovery. However, after 48 h, AT activity considerably exceeded control levels. A 5-fold decrease in the amount of administered meDNA resulted in the absence of its effect, whereas administration of higher amounts produced a further AT inactivation. A similar treatment with non-methylated DNA did not change AT activity. The possibility of AT exhaustion under in vivo conditions and thereby inhibition of repair of O6-alkylguanine in DNA, playing a key role in mutagenic, carcinogenic and antineoplastic effects of certain alkylating agents, might be helpful in increasing susceptibility of animals to such compounds.
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