Cycloleucine-induced vacuolation of myelin is associated with inhibition of protein methylation

Abstract

Chickens injected with cycloleucine developed vacuolation of myelin similar to that seen in humans with vitamin B 12 deficiency. Cycloleucine, an inhibitor of the formation of S-adenosylmethionine, decreased the incorporation of methyl groups into methylarginine in myelin basic protein in vivo. The need for methylcobalamin for the conversion of homocysteine to methionine and the requirement that myelin basic protein be methylated, offer a rational explanation for the myelin lesions observed in cases of vitamin B 12 deficiency where there is increasing evidence that methyl-, rather than adenosylcobalamin is required to prevent dysmyelination.