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It was found in white rats that hyperthyreosis (0.5% thyreoidin in dry food), respectively 2,4-dinitrophenol (30 mg/kg body weight/day i. p.), deficiency of the vitamins K and E or complete fasting increase the content of creatine in muscle, plasma and urine, but reduce the concentration of creatinine. Simultaneously the elevated creatine level of blood causes a repression of transamidinase in kidneys and pancreas. The common mode of action of the mentioned agents is seen in a decoupling of the oxidative phosphorylation, and in an insufficient availability of ATP, respectively.
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Infusion of dinitrophenol intra-arterially into rat hind limb caused an irreversible failure of isometric twitch tension and the induction of a severe progressive contracture. Metabolite analysis of muscle in which the twitch response had grossly fatigued revealed low levels of ATP and phosphocreatine together with lactate accumulation. Studies using 31P-n.m.r. confirmed the decrease in ATP and creatine phosphate concentrations and indicated a fall in intracellular pH. It is concluded that dinitrophenol-induced myopathy does not represent a good model for the human mitochondrial myopathic condition as has been previously suggested.