Cyclosporin A-induced functional and morphological changes in pilocarpine treated rat submandibular glands.

The effects of long-term administration of Cyclosporin A (CSA), an immunosuppressive agent, on submandibular glands of male albino rats were investigated. Sialochemistry studies revealed a reduction of pilocarpine-stimulated flow rates to 54% compared to the controls. Salivary Mg(2+) and K+ were elevated and a marked decrease in total protein concentration was observed.

Ultrastructural localization of calcium in neuromuscular junctions of smooth and skeletal muscles after aminoglycoside antibiotics treatment.

Aminoglycoside antibiotics are all capable of producing clinically significant neuromuscular paralysis. Since part of the mechanism of action of these antibiotics at neuromuscular junction is a calcium-dependent inhibition of acetylcholine release, so this experiment was carried out in vitro on both somatic (isolated rat phrenic-nerve hemidiaphragm) and autonomic neuro-effector transmission (guinea-pig ileum) using gentamicin and amikacin, to determine the calcium contents at this level. Electron microscopic observations on gentamycin- and/or amikacin-treated materials, using potassium pyroantimonate method suggest a reduction of internal calcium in nerve terminals of both preparations.

Inhibition of gentamicin-induced nephrotoxicity by lithium in rat.

Daily intraperitoneal injection of gentamicin in doses of 2, 4 and 10 mg/kg/day for 5 consecutive days produced proximal tubular necrosis in male albino rats as assessed by ultrastructural findings from electron microscopic observations. With respect to nephrotoxicity, aminoglycoside antibiotics (AGs) have been shown to concentrate in the lysosomes of kidney proximal tubular cells to inhibit the activities of phospholipases A and C, including a phospholipidosis, characterized by the formation of myeloid bodies. It has been suggested that the nephrotoxicity of AGs is related to the extent of this phospholipidosis.