Nutritional effect of possible intermediates of phytosterol dealkylation in the silkworm, Bombyx mori.
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Biomedical subjects
N Awata
Publications and source records attributed to N Awata.
Protective effect of taurine against isoprenaline-induced myocardial damage.
The effect of the sulfur amino acid, taurine, was examined on histological and biochemical changes induced by a toxic dose of isoprenaline in chick hearts. Isoprenaline treatment (80 or 240 mg/kg id twice daily for 4 days) caused a dose-dependent increase in heart weight and decrease in myocardial ATP. Isoprenaline administration (240 mg/kg id twice daily) produced necrotic changes in hearts, such as eosinophilic degeneration, myolysis, interstitial oedema, fibrosis, and inflammatory cell infiltration. Substantial accumulation of calcium was also observed. Taurine content of the heart was not significantly decreased. Parenteral administration of taurine (200 mg/day for 7 days) partially protected against these necrotic changes induced by isoprenaline. It is suggested that the protective effect of taurine against isoprenaline-induced myocardial injury might be due in part to the prevention of the massive overloading with calcium which is thought to cause myocardial cell necrosis.
Adenosine Triphosphate↗
Beneficial effect of coenzyme Q on myocardial slow action potentials in hearts subjected to decreased perfusion pressure-hypoxia-substrate-free perfusion.
Coenzyme Q, an important component of the electron transfer system in mitochondria, plays a central role in energy production aerobically. The effect of pretreatment with coenzyme Q10 (Co Q) on myocardial slow action potentials (APs) and accompanying contractions and on myocardial high energy phosphate content was studied in perfused hearts subjected to decreased perfusion pressure-hypoxia-substrate-free. Post-hatched chicks were treated i.p. with 10 mg/kg of Co Q daily for 5 days. To study the slow APs exclusively, the fast Na+ channels were voltage-inactivated by elevated K+ (25 mM) Tyrode solution. The Ca++-dependent slow APs were induced by elevating [Ca]o to 5.4 mM; hearts were paced at a rate of 40 per min. Hearts which had been pretreated with Co Q were protected against the deleterious effect of decreased perfusion pressure - hypoxia - substrate-free perfusion on mechanical performance accompanying the slow Ca++-Na+ APs. The slow APs in hearts pretreated with Co Q were also less affected than were non-treated hearts. However, the myocardial ATP and total adenine nucleotides were not affected by exogenous Co Q. It was suggested that exogenous Co Q could protect against the decline of cardiac contractions via improved availability of slow APs during decreased perfusion pressure - hypoxia - substrate-free, independently of the cellular high energy phosphate level.
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