Reduction by coenzyme Q10 of the acute toxicity of adriamycin in mice.

Pretreatment for four days with coenzyme Q10 (COQ10) reduced the acute toxicity in mice treated with adriamycin. In two sequential protocols, adriamycin allowed only 36 and 42% survival, respectively. Pretreatment with COQ10 allowed 80 and 86% survival, respectively.

In vitro photodecomposition of uric acid in presence of riboflavin II.

In vitro studies on the photodecomposition of uric acid in the presence of the monosodium salt of riboflavin 5'-phosphate in buffers at various pH values, in methanol, and in human plasma are reported. The decomposition rate increased with increasing pH and was independent of solvent or buffer species. The mechanism appears to be an energy transfer process involving triplet riboflavin and single oxygen.

The lithium librarian. An international index.

Lithium salts are being widely used for treatment and prophylaxis of bipolar affective disorder (manic-depressive psychosis) and are under investigation in more than 30 other illnesses. The relevant literature has grown from 43 articles published between 1949 and 1964 to nearly 4,000 today. A computer-based lithium librarian program has been developed that provides an up-to-date registry of all lithium references, rapid search capability, constant availability, and easy transferability to identical computer systems located on three continents.

Effects of exercise training and exhaustion on 45Ca uptake by rat skeletal muscle mitochondria and sarcoplasmic reticulum.

Mitochondrial and sarcoplasmic reticular 45Ca2+ uptake and Ca2+-ATPase activity were determined in skeletal muscle from exercise trained and non-trained rats at rest or following short-term exhaustive exercise. In trained rats exercised to exhaustion, mitochondrial 45Ca2+ uptake was significantly depressed when compared to non-trained rats at rest. Ca2+-ATPase activity of sarcoplasmic reticulum from trained rats exercised to exhaustion was significantly increased as compared to trained rats at rest.

Models for clinical disease. I. Biochemical cardiotoxicity of a coenzyme Q10-inhibitor in rats.

The pharmacology and toxicity in animals of synthetic analogs of essential metabolites, which show in vitro antagonism of the metabolite, may point out pathology associated with a deficiency of the metabolite. On this basis, 2-hydroxy-3-n-dodecylmercapto-1,4-naphthoquinone, a potent in vitro inhibitor of a mitochondrial coenzyme Q10-enzyme, was administered to rats. The specific activities and the percent deficiencies of the succinate dehydrogenase-coenzyme Q10 reductase in cardiac mitochondria were significantly increased (0.

Anticoagulant activity of a naphthoquinone analog of vitamin K and an inhibitor of coenzyme Q10- enzyme systems.

Synthetic 2-hydroxy-3-h-dodecylmercapto-1,4-naphthoquinone is an analog of both vitamin K1 and coenzyme Q10. This naphthoquinone analog is an effective inhibitor of coenzyme Q10-enzymes of mammalian mitochondria, which are components of electron transfer mechanisms of respiration and coupled oxidative phosphorylation. This analog increased the prothrombin time in rats when it was administered orally or parenterally.

The action of isoproterenol on phenylthiourea induced pulmonary edema.

Isoproterenol inhalation increases the pulmonary edema induced in rats by phenylthiourea. Propranolol decreases this response while phenoxybenzamine has no effect upon it. It is proposed that the observed increase in toxicity is related to the beta-adrenergic effects of the isoproterenol and that the specific mechanism responsible might be an increase in pulmonary capillary hydrostatic pressure which is secondary to an increase in pulmonary blood flow.