Preservation of shock-wave-induced renal histologic changes by dermatan sulfate

Hyperoxaluria-induced tubular ischemia: the effect of verapamil on the limitation of tissue HIF-1 alpha levels in renal parenchyma

“…Additionally, allopurinol as well as vitamin E has been used as antioxidant agents to prevent the deleterious effects of free radicals in parenchymatous organs. These reported findings indicate the possible effects of tubular ischemia induced by ROS formation as a result of hyperoxaluric phase in renal tubules [10][11][12].…”

Morphological changes induced in the pig kidney by extracorporeal shock wave lithotripsy: Nephron injury

“…In addition, other researchers proposed that oxidative stress associated with ischemia induced by SWL may also contribute to the resulting tissue injury (Sarica et al, 1996a;Cohen et al, 1998;Brown et al, 2000;Munver et al, 2002). Support for a possible role of oxidative stress in the tubular injury caused by shock waves comes from several studies in which inhibitors of oxidative stress reduced the urinary excretion of enzymatic markers of tubular injury (Strohmaier et al, 1991(Strohmaier et al, , 1993(Strohmaier et al, , 1994a(Strohmaier et al, , b, 1999(Strohmaier et al, , 2002Benyi et al, 1995;Ogiste et al, 2003) or diminished the histological signs of tissue injury (Fegan et al, 1991;Yaman et al, 1996;Sarica et al, 1997;Biri et al, 1998) after SWL. The precise role of oxidative stress in shock wave-induced injury (i.e., cause or effect, both, or none) remains to be determined.…”

Limitation of apoptotic changes and crystal deposition by Tutukon following hyperoxaluria-induced tubular cell injury in rat model

“…Among the agents used so far, verapamil and nifedipine (calcium channel blockers) were found to limit histologic changes and crystal deposition to a certain extent [12,19,20]. Potassium citrate again was found to limit stone recurrence after extracorporeal shockwave lithotripsy [7], and as highly potent antioxidant agents, allopurinol and vitamin E have been used to minimize free oxygen radical-induced alterations in certain tissues by inhibiting ROS formation [11,13,14,21].…”

“…Apart from possible hyperoxaluria-induced tubular ischemia, which gives rise to ROS production as a result of lipid peroxidation, studies have Abstract This study aimed at evaluating the protective effects of a herbal medication (Tutukon) on the hyperoxaluria induced apoptotic changes and crystal deposition in renal tubular epithelium in rat model. 60 male wistar rats were divided into three different groups (each group n: 20). In Group I severe hyperoxaluria was induced by ethylene glycol (EG) (0.75 %) administration for 28 days.…”