and LDM) is dependent on the amount of radiation applied [14,16,17]. It was shown (hat the anti-complement and platelet-aggregating effect (indicating membrane damage) of detoxified endotoxin was partly maintained [ 1 $], which was dependent on the radiation dose used (Fig. 2). The decrease of membrane perturbation by radiated LPS was proven in these studies by the measurement of 3H-concanavalin binding [19]. Table I shows the comparison of major effects

Figure 2. Effect ot endotoxin (LPS) and radiodeloxilied endotoxin (RD-I.PS: 150 kGy) on human thrombocytes (in vitro). Scanning el eel ion microscopic studies (15000X) <n=5). (a) unhealed, (b) LPS-treated, (c) RD-LPS-treated [18],

of LPS and RD-LPS.

It was demonstrated in mice ihal toxic LPS increased ¡he blood level of very low density lipoprotein (VLDL) whereas the RD-LPS did not, indicating lhal hyperlipidaemia is a marker of LPS toxicity [20J, We also found that RD-LPS inhibited membrane-bound adenylate cyclase (AC) less than its toxic counterpart [2 i ].

Depending on the radial ion dose used, RD-LPS preparations do not release or show a decreased release of lysosomal enzymes (heia-glucuronidase, c at h opsin D). The capacity to induce ¡he Sanarelli-Shwartzman reaction was decreased by half, as was pro-coagulant activity as measured with rabbit leukocytes [8,22,23

We found that radiation treatment of mice (10 Ciy; ^Co-gamma) significantly increased their LPS sensitivity and 300 ttg doses led to i00% mortality on days 3 and 7 after treatment, whereas identical doses of RD-LPS induced no ill effects. 1( was also observed that animals bearing Lewis lung carcinomas showed increased sensitivity to LPS but RD-LPS had no ill effects in such animals |24], li is long recognized that bacterial endotoxins have significant metabolic effects. In the liver microsomal monooxygenase enzyme systems are sensitive to endotoxin [25], Because of the potential anti-shock effect of RD-LPS, we examined its effect on the microsomal monooxygenase system. The metabolic in activation of narcotic agents is dependent on microsomal enzyme activity. We demonstrated that RD-LPS, in contrast with loxie LPS, exerts a significantly decreased inhibitory effect on liver microsomal mono-oxygenase enzymes. In LPS-trealed animals phen»barbital was unable to induce these enzymes, whereas in RD-LPS (150 kGy) treated animals enzyme induclion was present. The mechanism of enzyme inhibition by LPS is unknown, It is possible lhal LPS damages the cytochrome P-450 enzyme 123],

We studied ihe mechanism of endotoxin detoxification by radia!ion. It was indicated that a dose-dependent induction of free radicals in the water phase induced or led to the induction of structural changes in endotoxin. This led to (he decrease of glucosamine, keto-deoxy-octonic acid and laity acids [26,27J. Ionizing radiation has been used in several other laboratories for the detoxification of endotoxin and confirmed our observations [17,28-32J.

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