'Oxygen toxicity' induced by isoproterenol oxidation on living cells. An in vitro prokaryotic model.

Oxygen radical damage is a relevant problem in gerontological research. It has been implicated both in the aging process itself and in aging-related pathologies. Oxygen radicals from catecholamines seem to play an important role in central nervous system and cardiovascular system disorders during aging. Prokaryotic experimental systems have been shown to provide a simple and short term in vitro model for 'oxygen toxicity' from catecholamine oxidation which might be useful also in age-related research. In this paper we show that the synthetic sympathomimetic catecholamine, isoproterenol, oxidizes when added to bacteriological media and that this oxidation process causes bacterial growth inhibition. Both isoproterenol oxidation and the growth-inhibitory activity can be prevented by the addition of antioxidants. The addition of exogenous catalase (CAT), while unable to prevent isoproterenol oxidation, totally suppressed the bacterial growth inhibition; the addition of exogenous superoxide dismutase partially antagonized isoproterenol oxidation and suppressed bacterial growth inhibition although less efficiently than CAT. The model described suggests that besides 'oxygen toxicity' by endogenous natural catecholamines, iatrogenic tissue injury caused by the oxidation intermediates from this class of pharmacological compounds must also be considered.