ABSTRACT
Male Wistar rats were sacrificed 12 weeks after single exposure to various organophosphate compounds. Peripheral nerves and skeletal muscles were examined light microscopically for the occurrence of a delayed polyneuropathy. Although unequivocal morphological hallmarks of OPIDN had been demonstrated in other rat strains using similar doses of TOCP or mipafox, we were unable to demonstrate any abnormality with these compounds. Normal findings were also obtained with fenthion, the delayed neuropathic potential of which is debated, and with paraoxon or parathion, which are both highly unlikely to cause OPIDN. These data indicate that the Wistar rat strain is highly likely to be resistant to OPIDN.
Subject(s)
Disease Models, Animal , Organophosphorus Compounds/toxicity , Peripheral Nervous System Diseases/chemically induced , Rats, Wistar , Animals , Disease Susceptibility , Male , Peripheral Nerves , RatsABSTRACT
We studied the incidence of paraoxon-induced myopathy in several rat skeletal muscles in relation to the morphometric properties and oxidative metabolism of their fibers. The necrosis was most pronounced in the predominantly oxidative-rich fiber-composed diaphragm. The purely oxidative-rich masseter and soleus muscles were also severely affected. All 7 mixed muscles with oxidative-poor fiber predominance were far less involved. A high correlation between oxidative capacity and the extent of the muscle fiber necrosis was evidenced in mixed muscles. No relation was found between the muscle fiber diameter and the susceptibility to necrosis. We conclude that muscles predominantly composed of highly oxidative fiber types are more susceptible to organophosphate-induced necrotizing myopathy. Oxidative capacity alone is not the only factor, however, as the mixed diaphragm was more involved than the purely oxidative-rich masseter and soleus. Several features of the distinct fiber types could be responsible for the variable vulnerability.
