[Incorporation of 2-14C-acetate into the glycolipids of the spinal cord and brain stem of normal guinea pigs and guinea pigs in the paralytic stage of triorthocresylphosphate poisoning].

Paralytical form of chronic intoxication was caused by single intracutaneous administration of tri-O-cresyl phosphate (TOCP)/2=2.2 ml/kg/ into guinea pigs. Within the first 27--33 days after the treatment, the animals with pronounced symptoms of neurotoxic effect of TOCP were subcutaneously administered with 2-14C-acetate/100 mu Ci per 100 g of body weight/2 hrs before decapitation. Purified cerebrosides, gangliosides and acid-soluble fraction, containing 14C-precursors, were isolated and their specific radiactivity was measured in a gas-flow counter. The rate of 14C incorporation into cerebrosides and gangliosides in spinal cord was found to exceed that in brain stem. In paralytical stage of disease, caused by TOCP, synthesis of cerebroside was depressed in spinal cord and in brain stem, according to calculated value for relative specific radioactivity. In spinal cord the rate of 14C incorporation into gangliosides was also decreased. These data suggest that neurtoxic drug TOCP affects metabolic processes both in oligodendroglial cells and in neurons, where ganglioside biosynthesis occurs.