Особливості морфології фетальної печінки щурів під впливом ацетату свинцю та за умов корекції наносріблом

Abstract

Введення вагітним самицям щура розчину ацетату свинцю в дозі 0,05 мг/кг призводить до гепатотоксичних проявів у ембріонів. Негативний вплив ацетату свинцю на ембріональну печінку визначався у збільшенні кількості сінусоїдів и центральних вен паренхіми печінки. Під впливом цитрату срібла на тлі свинцевого впливу послаблюється оксидативний стрес, відновлюються процеси дозрівання та диференціювання печінки. Таким чином, цитрат срібла на тлі свинцевої інтоксикації в період гепатогенезу має модифікуючу дію і може розглядатися як біоантогоніст гепатотоксичності ацетату свинцю.

Введение беременным самкам крыс раствора ацетата свинца в дозе 0,05 мг/кг приводит к гепатотоксических проявлений у эмбрионов. Негативное влияние ацетата свинца на эмбриональную печень проявляется в увеличении количества синусоидов и центральных вен паренхимы печени. Усиление их кровенаполнения свидетельствует о развитии гипоксии под действием низких доз солей данного металла. Под влиянием цитрата серебра на фоне свинцового воздействия ослабляется оксидативный стресс, восстанавливаются процессы созревания и дифференцировки печени. Таким образом, цитрат серебра на фоне свинцовой интоксикации в период гепатогенеза имеет модифицирующее действие и может рассматриваться как биоантогонист гепатотоксичности ацетата свинца.

The aim of the study was to investigate the morphology of embryonic liver under the influence of silver citrate on a background of lead intoxication. All rats were divided into 4 groups: Group K (control) – animals that received the distilled water; group Pb – animals treated with a solution of lead acetate at a dose of 0.05 mg/kg; group Pb + Ag – animals treated with a solution of lead acetate at a dose of 0.05 mg/kg and a solution of silver citrate at a dose of 2 mg/kg; group Ag – animals treated with a solution of silver citrate at a dose of 2 mg/kg. Each group was divided into two groups – one of which is deduced from the experiment at day 16 of pregnancy, while the other – on the 20th day. After surgical slaughter fetuses were removed from the uterus and fixed in 10% neutral formalin solution for further morphometric and histological examination. After fixing the liver was removed from the embryo and weighed. Histological specimens were stained with hematoxylin and eosin. Microscopically embryonic rat liver has no distinct lobular structure. Connective tissue layer is not developed, portal areas are not detected. At 16 and 20 days of embryonic development is determined a future central vein with erythrocytes. Cells of erythroid precursor on 16 day of embryoinic development of liver were contained nucleus. Red blood cells were formed to 20 day of development and were not contained nuclei. Sinusoidal capillaries dilated unevenly and don’t have clear radial orientation. Hematopoietic cells were located extravasculary, which at 16 days of embryogenesis have form of strands, while on the 20th day they are located like islands, due to the disintegration of hematopoietic cells in late embryonic development. At 16 and 20 days of liver development the hepatocytes don’t have typical polygonal shape, don’t form distinct beams and cells form winding strands without a clear radial orientation, probably due to the performance of liver hematopoietic function during embryonic period, while in postnatal period liver has digestive function. Structural organization embryonic liver of rats whose mothers received lead acetate during pregnancy, while visual assessment is not materially different. In assessing liver histological sections 16 and 20 day don’t have mature hepatic lobules, connective tissue layers visually is not seen, the beams are not formed, but the future central vein is detected. Sinusoid extended compared with the control group, full-blooded, the number of vessels increased significantly compared with the control, that indicates manifestation of oxidative stress caused by lead. Hematopoietic islands are found in liver parenchyma, number of hematopoietic cells is much higher compared to the control group. Hepatocytes are single on 16 day of development, and theirs number on 20 day is much smaller compared with the control group. In our opinion, it shows delayed maturation of the liver under the influence of lead acetate. Under the combined influence of lead acetate and silver citrate hepatic lobules are not found, hepatocyte bands don’t have a clear radial orientation, the connective tissue is not found. Sinusoidal capillaries unevenly expanded, reduced the number of vessels compared with the group of lead intoxication. Visually, the number of hematopoietic cells is much lower compared with the group of lead exposure. Number of hepatocytes is higher compared with the group of lead intoxication and close to the level of control numbers. We think, this fact indicates improvement of processes of growth and development under the influence of silver citrate on a background of lead intoxication. Under the influence of silver citrate against the background of lead exposure, oxidative stress is weakened, the processes of maturation and differentiation of the liver are restored. Thus, silver citrate against the background of lead intoxication during hepatogenesis has a modifying effect and can be considered as a bioanthonist of the hepatotoxicity of lead acetate.