mechanisms of this phenomenon.The effect of Ca ++ is evidently not mediated by calmodulin, for it is unchanged by trifluoperazine.The impression is gained that Ca ++ acts directly on ICDH. However, more complex mechanisms cannot yet be ruled out: phosphorylation of some unknown protein intermediary or the participation of another Ca++-receptive protein.For instance, it has recently been shown that phosphorylation of a mitochondrial protein with molecular weight of 3500 daltons is increased by glucagon [12]. Ca++ metabolism in the mitochondria is modified by stimulators not only of a-adrenoreceptors, but also of B-adrenoreceptors [5], and also by cAMP [8]. Perhaps Ca ++ ions activate ICDH through the intermediary of catecholamines and cAMP. LITERATURE CITED I. T. V. Kolpakova and V. V. Mezhevikin, in: Regulatory Effects and Metabolism of Monoamines and CyclicAn important aspect of the study of the effect of cholera toxin (CT) in vivo is the state of the detoxication enzyme system (DES). This system has evolved in order to activate potentially harmful cytotoxic substances formed during metabolism and to render harmless toxins entering from outside.The first function has been studied reasonably well. Activity of enzymes of the mono-oxygenase system (stage I of detoxication) and activity of epoxide hydratase (EH) and glutathione-SH-transferase (GT) (stage II) has been investigated in the liver, kidneys, lungs, and intestine [4, 5, i0, 13], and in the blood cells [12]. The second function of DES is only beginning to be investigated [6,8]. In our view, to understand the role of the antitoxic system in mobilization of the defensive forces of the body in infectious pathology it is essential to examine the state of those of its enzymes, such as EH, cytochrome-450, uridine disphophoglucuronyl-transferase, GT, superoxide dismutase (SOD), and glutathione peroxidase (GP), in the small intestine, which is the target for bacterial toxins, and also in the liver, the principal detoxicating organ.The aim of this investigation was to study the principal enzyme of nonspecific defense of the body against the toxic action of oxygen (SOD) and of GP in cytosols of the mucous membrane of the small intestine and in the liver of rats exposed to the action of CT.
