Correction of Oxidative Stress in Gastric Mucosa of Rats by Enterosorbents of Different Classes During Chronic Nitrate Fluoride Intoxication

Abstract

In some regions of Ukraine, the environmental conditions can be considered as threatening for the life of people and animals. There has been reported excessive accumulation of nitrates in the bodies of humans and animals with food and drinking water in regions with developed agriculture. At the same time, in regions with developed chemical and metallurgical (especially aluminium production) industries, additional contamination of drinking water with excess fluoride has been found out to take place. Thus, simultaneous excess intake of nitrates and fluorides into the human body cannot be excluded. The purpose of this work is to determine the effect of nanosized silica, Carboline and hydrolytic lignin suspensions on the production of superoxide anion radical (О2∙-), the activity of antioxidant enzymes, the content of oxidative-modified proteins and the concentration of primary products of lipid peroxidation (POL). Materials and methods. All biochemical studies were carried out in 10% gastric mucosa homogenates of the rats. The study assessed the activity of superoxide dismutase (SOD), catalase, content of diene conjugates, octadiene conjugates, trien conjugates, the content of oxidative-modified proteins (OMP) and О2∙- production. Results. Chronic nitrate-fluoride intoxication leads to an increase in the basic О2∙- production with a simultaneous decrease in the activities of SOD and catalase. The content of primary POL and OMB increases during chronic intoxication. Usage of enterosorbent suspensions reduces О2∙- production, restores functioning of antioxidant enzymes, lowered the content of primary POL and OMP. Conclusions. Chronic nitrate-fluoride intoxication leads to oxidative damage to the phospholipids of biological membranes and the protein structures of the gastric mucosa. Suspensions of nanosized silicon oxide, carboline and lignin are effective means for correcting oxidative damage to the gastric mucosa during chronic nitrate-fluoride intoxication.

Intensity of Nitric Oxide Synthesis in the Blood of Rats Under the Influence of Sodium Fluoride

“…Typically, excess levels of terminal stable NO metabolites are associated with overexpression of the inducible isoform of NO synthase (iNOS) resulting from oxidative stress. iNOS produces NO in an amount that is several orders of magnitude higher than the production of NO by the endothelial isoform of NO synthase and causes the stimulation of the formation of free radicals [7]. As a result, a larger amount of NO is formed, which is confirmed by an increase in the content of its final products.…”

“…At low NO concentrations, direct effects aimed at maintaining homeostasis, such as the vascular, respiratory, and nervous systems, predominate; at high concentrations of NO, indirect effects prevail, due primarily to the formation of peroxynitrite. It is known that when the rate of free radical reactions in the body increases, NO can react with the superoxide anion radical to form peroxynitrite, a highly reactive compound with destructive properties in relation to proteins and lipids [7].…”

The state of oxidative-antioxidant homeostasis under the influence of subtoxic doses of sodium fluoride

“…A direct relationship was noted between the level of free radical oxidation of lipid systems in the body and the intensity of CL of biological systems [6,21]. In this case, the change in the intensity of blood BCL can be considered as an integral reaction of the body, which makes it possible to judge the nature of molecular and electronic disorders of biological structures under various physiological conditions and pathological processes.…”

Інтенсивність Синтезу Оксиду Азоту У Крові Щурів Під Впливом Фториду Натрію

“…При низьких концентраціях NO переважають прямі ефекти, спрямовані на підтримку гомеостазу, наприклад, судинної, дихальної та нервової систем; при високих концентраціях NO -переважають непрямі ефекти, зумовлені, перш за все, утворенням пероксинітриту. Відомо, що при підвищенні в організмі швидкості вільнорадикальних реакцій NO може вступати у реакцію з супероксидним аніон-радикалом з утворенням пероксинітриту -високо реакційної сполуки з деструктивними властивостями по відношенню до білків і ліпідів [7].…”

“…Як правило, надлишковий рівень кінцевих стабільних метаболітів NO пов'язують з гіперекспресією індуцибельної ізоформи NO-синтази (iNOS), що виникає в результаті оксида-тивного стресу. iNOS продукує NO у кількості, що на кілька порядків перевищує продукцію NO ендотеліальною ізоформою NO-синтази та зумовлює стимулювання утворення вільних радикалів [7]. У результаті утворюється більша за норми кількість NO, що підтверджується збільшенням вмісту його кінцевих продуктів.…”