Key result
Vitamin K1 administration restored prothrombin levels in deficient rats, indicating its function occurs at a late stage in the translation of prothrombin mRNA rather than at the genetic level.
This preclinical study demonstrates that vitamin K functions at a late stage in the translation of prothrombin mRNA to form a functional prothrombin molecule, rather than at the genetic transcription level.
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Supports vitamin K acting at late mRNA translation in prothrombin synthesis; leaves open relevance to human coagulation disorders.
The role of vitamin K in the synthesis of prothrombin has been examined with the following results. 1. Vitamin K deficiency has no effect on general protein synthesis as studied by amino acid incorporation into protein in vivo and in vitro and by tryptophan pyrrolase production following tryptophan feeding. 2. Prothrombin activity was found in normal rat liver microsomes with increased release following ultrasonic treatment, but could not be found in microsomes from the livers of vitamin K-deficient rats or dicumarol-treated rats. Administration of suboptimal levels of vitamin K to vitamin K-deficient rats resulted in detectable microsomal prothrombin in 2 hours and essentially normal values within 3 hours. 3. Adequate vitamin K1, given by injection, completely restored the blood prothrombin levels of vitamin K-deficient rats in 1 hour, and of dicumarol- or warfarin-treated rats in 5 to 7 hours depending on the amounts of warfarin and vitamin K1 given. 4. Following administration of actinomycin D or ethionine to vitamin K-deficient rats, treatment with vitamin K1 markedly stimulated prothrombin production, indicating that the site of action of vitamin K is beyond the level of transcription of DNA to prothrombin messenger RNA. 5. Treatment with vitamin K1, following administration to vitamin K-deficient rats of cycloheximide at a level just sufficient to block synthesis of prothrombin for 6 to 8 hours, gave an essentially normal prothrombin response. At higher cycloheximide levels the response to vitamin K1, while much less complete, was clear and definite. 6. The response of vitamin K-deficient rats to vitamin K1, administered following treatment with blocking doses of puromycin, appears significant. 7. These data appear to indicate that the site of function of vitamin K is not at the genetic level, as has been reported, but at a late stage in translation of prothrombin messenger RNA to form a functional prothrombin molecule.
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Hill et al. (1968) studied Vitamin K deficiency. Vitamin K1 was evaluated on Prothrombin synthesis and activity. Vitamin K1 administration restored prothrombin levels in deficient rats, indicating its function occurs at a late stage in the translation of prothrombin mRNA rather than at the genetic level.
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