Nitric oxide synthase activity and peroxynitrite content in cells of rat’s mucous coat of stomach under experimental stress-induced ulcer

Досліджено активність синтази оксиду азоту та рівень пероксинітриту у клітинах слизової оболонки шлунка щурів за умов експериментальної моделі стресової виразки. За умов дії стресового чинника активність синтази оксиду азоту зростає, що призводить до збільшення кількості пероксинітриту та супроводжується формуванням виразкових дефектів. Ступінь ураженості слизової обо­лон­ки шлунка залежить від тривалості дії пошкоджувального фактора. Показано, що оксид азоту залучений до складних патогенетичних механізмів виразкоутворення.Исследована активность синтазы оксида азота и уровень пероксинитрита в клетках слизистой оболочки желудка крыс при экспериментальной модели стрессовой язвы. В условиях действия стрессового фактора активность синтазы оксида азота возрастает, что приводит к увеличению количества пероксинитрита и сопровождается формированием язвенных дефектов. Степень пораженности слизистой обо¬лон¬кы желудка зависит от продолжительности действия повреждающего фактора. Показано, что оксид азота вовлечен в сложных патогенетических механизмов язвообразования.Nitric oxide synthase activity in gastric mucosal cells as well as peroxynitrite generation in experimental stress-induced gastric ulcer formation in rats were studied. There was made the conclusion that nitric oxide synthase activity is growing during the stress. It causes increasing of peroxynitrite’ production and ulcer formation. It was established that destructive gastric mucosal damages depend on stress’ duration. It was determined that nitric oxide is involved in complex pathogenetic mechanisms of ulceration

Meat Intake and the Dose of Vitamin B3 - Nicotinamide:Cause of the Causes of Disease Transitions, Health Divides, and Health Futures?

Meat and vitamin B 3 – nicotinamide – intake was high during hunter-gatherer times. Intake then fell and variances increased during and after the Neolithic agricultural revolution. Health, height, and IQ deteriorated. Low dietary doses are buffered by ‘welcoming’ gut symbionts and tuberculosis that can supply nicotinamide, but this co-evolved homeostatic metagenomic strategy risks dysbioses and impaired resistance to pathogens. Vitamin B 3 deficiency may now be common among the poor billions on a low-meat diet. Disease transitions to non-communicable inflammatory disorders (but longer lives) may be driven by positive ‘meat transitions’. High doses of nicotinamide lead to reduced regulatory T cells and immune intolerance. Loss of no longer needed symbiotic ‘old friends’ compounds immunological over-reactivity to cause allergic and auto-immune diseases. Inhibition of nicotinamide adenine dinucleotide consumers and loss of methyl groups or production of toxins may cause cancers, metabolic toxicity, or neurodegeneration. An optimal dosage of vitamin B 3 could lead to better health, but such a preventive approach needs more equitable meat distribution. Some people may require personalised doses depending on genetic make-up or, temporarily, when under stress

Aктивність синтази оксиду азоту та вміст пероксинітриту у клітинах слизової оболонки шлунка щурів за умов експериментальної стресової виразки

Nitric oxide synthase activity in gastric mucosal cells as well as peroxynitrite generation in experimental stress-induced gastric ulcer formation in rats were studied. There was made the conclusion that nitric oxide synthase activity is growing during the stress. It causes increasing of peroxynitrite’ production and ulcer formation. It was established that destructive gastric mucosal damages depend on stress’ duration. It was determined that nitric oxide is involved in complex pathogenetic mechanisms of ulceration

NAD+ Is a Food Component That Promotes Exit from Dauer Diapause in Caenorhabditis elegans.

The free-living soil nematode Caenorhabditis elegans adapts its development to the availability of food. When food is scarce and population density is high, worms enter a developmentally arrested non-feeding diapause stage specialized for long-term survival called the dauer larva. When food becomes available, they exit from the dauer stage, resume growth and reproduction. It has been postulated that compound(s) present in food, referred to as the "food signal", promote exit from the dauer stage. In this study, we have identified NAD+ as a component of bacterial extract that promotes dauer exit. NAD+, when dissolved in alkaline medium, causes opening of the mouth and ingestion of food. We also show that to initiate exit from the dauer stage in response to NAD+ worms require production of serotonin. Thus, C. elegans can use redox cofactors produced by dietary organisms to sense food