Modern aspects of regulatory, pathophysiological and toxic effects of cobalt ions during oral intake in the human body

Cobalt is an essential microelement which is an indispensable part of several enzymes and co-enzymes. Cobalt ions may occur in the environment from both natural sources and due to human activities. This metal is very widespread in the natural environment and can be formed due to anthropogenic activity. Toxic effects produced by cobalt and its compounds depend on the physical and chemical properties of these complexes, including their electronic structure, ion parameters (charge-size relations) and kinetics. Cobalt has both beneficial and harmful effects on human health. Cobalt is beneficial for humans because it is a part of vitamin B12, which is essential to maintain human health. If humans and animals are exposed to levels of cobalt normally found in the environment, it is not harmful. When excessive cobalt amounts enter a human body, multiple and chronic harmful health effects can occur and the longer the cobalt ions are stored in the body, the more changes they cause in cells. Cobalt gets into a body via several ways: mainly with food, via the respiratory system, through the skin or as a component of various biomaterials. Despite this metal being abundant, much of our knowledge on cobalt toxicity is based mainly on studies performed on animals. Undoubtedly, inorganic forms of cobalt are toxic as they accumulate in various tissues and can evoke a chain of pathological cascade changes in cells. Although some cobalt effects might be beneficial for medicine. Therefore, the purpose of our review is to provide the current analysis about the most significant regulatory, pathophysiological and epigenetic effects of Co2+ in a human body

The influence of iodine-131 on the functional state of the kidneys in albino rats

На білих щурах досліджувався стан кислотовидільної та іонорегулюючої функції нирок за надходження до організму 131I в кількості 2 МБк/кг маси тіла. Стан судинно-клубочкового апарату оцінювали за екскрецією креатиніну, діяльність канальцевого відділу розцінювали за екскрецією електролітів, титрованих кислот і аміаку. Нефротоксичні ефекти радіойоду переважно локалізовані на рівні судинно-клубочкового апарату. Порушення канальцевих процесів транспорту катіонів під впливом 131I призводить до зниження інтенсивності енергозалежних механізмів реабсорбції натрію і пошкодження натрій-водневого антипорту.The state of the acidproducing and ion-regulating renal functions after the administration of 131I in a quantity of 2 MBq/kg of body mass, has been investigated on white rats. The state of the vascular-glomerular apparatus was estimated by creatinine excretion, the activity of the tubular section was estimated by the excretion of electrolytes, titrated acids and ammonia. The nephrotoxic effects of radioiodine is mainly located at the level of the vascular-glomerular apparatus. Derangements of the tubular processes of the cation transport under the influence of 131I results in a decrease of the intensity of energy-dependent sodium reabsorption mechanisms and disturbance of the sodium-hydrogen antiport

Effect of 131I on the functional state of the kidneys in albino rats

Через 7 суток после введения 131I наблюдается достоверное снижение экскреции креатинина, увеличение стандартизированной экскреции калия, снижение экскреции протонов, повышение стандартизированных экскреций титруемых кислот и аммиака. Изменение канальцевых процессов транспорта под влиянием 131I обусловлено нарушением энергозависимой реабсорбции натрия. Вызванное радиойодом угнетение кислотовыделительной функции почки связано с нарушением натрий-водородного антипорта.A reliable decrease of creatinine excretion, a decrease of standardized potassium excretion, a reduction of proton excretion, an elevation of standardized excretions of titrated acids and ammonia were observed in 7 days after the administration of 131I. Alterations of transport tubular processes under the influence of 131I are due to a disorder of energy-dependent sodium reabsorption. An inhibition of the renal acid-producing function by means of radioiodine is connected with a disturbance of the sodium-hydrogen antiport