Histological, histochemical and ultrastructural changes in the kidneys and live of Red-eared sliders (Trachemys scripta elegans (Wied, 1839)) as a result of Gentamicin parenteral injection

Abstract

Reptiles belonging to the vertebrate poikilothermic animals quite often contract non-communicable, infectious and invasive diseases. The principles of treatment of reptiles differ significantly from drug therapy for mammals and birds. For the purpose of studying the nephro- and hepatotoxic effects of aminoglycosides, histological, histo- chemical and ultrastructural examinations of the kidneys and liver of Red-eared slider were conducted. The turtles were injected with gentamicin at a dose of 10 mg/kg into thoracic limb muscles. Histological sections were made using a sledge microtome and a cryostat. The histological sections were stained with hematoxylin and eosin as well as Sudan III, and the PAS staining was performed according to McManus. For the detection of DNA and RNA, the methyl green and pyronin staining according to Brachet was performed. The kidneys examination of Red-eared slider, which received gentamicin, revealed that most of the capillary loops of the renal glomeruli were spasmodic while the glomerular basement membranes were thickened and intensely PAS-positive. In some renal glomeruli, deformation and fusion of the adjacent haemocapillary loops were discovered. Transmission electron microscopy revealed structural changes in the filtration barrier, characterised by heterogeneous size of the cytoplasmic fenestras of the renal glomerular endothelial cells, swelling of cytopedicels and heterogeneous reduction in the width of filtration slits. The mesangial matrix was expanded, thickened, and hypercellular. Tubular damage of the renal tubuli was most pronounced in the proximal segments of the nephron and was characterised by the development of hyaline-drop and, in some nephrocytes, vacuolar dystrophy, necrosis and apoptosis. Ultrastructural examination of the proximal tubuli revealed destruction of the brush border, accumulation of cytosomes and phagosomes in the cytoplasm, damage to mitochondria. Degenerative changes in hepatocytes were characterised by a decrease in the number of glycogen granules, destruction of the rough endoplasmic reticulum ribosomes and a reduced RNA content of the cytoplasm of the hepatic parenchymal cells. Necrotic lesions of hepatocytes and the development of apoptosis were also detected. Dyscirculatory changes were characterised by the development of vessels hyperaemia of the venous bed of the liver.