Effects of Pentoxifylline on Amikacin-Induced Nephrotoxicity in Rats

Abstract

The nephrotoxicity of amikacin (AK) was prevented with pentoxifylline (PTX) in a rat model. Rats were received a single injection of AK (1.2 g/kg, i.p.) with or without PTX pretreatment (25 mg/kg, orally). Renal morphology was investigated by light microscopy. Tissue samples and trunk blood were also obtained to determine renal malondialdehyde (MDA), blood urea nitrogen (BUN), and creatinine (Cr) levels. MDA production was found to be higher in AK group. PTX administration caused a significant decrease in MDA production. Morphological damage in rats given AK was severe in the kidney, whereas in rats given AK plus PTX, no histological changes occurred. It is concluded that PTX could be useful for reducing the nephrotoxic effects of AK.

The Effect of Grape Seed Proanthocyanidin Extract in Preventing Amikacin-Induced Nephropathy

“…Gentamicin nephropathy models have been more extensively studied, using molecules including fish oil, 4 pentoxifylline, 5 green tea, 6 caffeic acid phenyl ester (CAPE), 7 vitamin E and vitamin C, 8 and GSPE, 11 (a) (A) and so on. The AK nephropathy model has been used in fewer studies, but the effects of antioxidant molecules including CAPE, 3 N-acetylcysteine (NAC), 9 melatonin, 22 and pentoxifylline 10 have been investigated. While alterations in oxidative system, as well as biochemical and histopathological changes have been examined in some of the studies, only biochemical and histopathological changes have been investigated in others.…”

“…4 Several experimental studies have been conducted in order to find a way to reduce AG-induced toxicity, and the effects of antioxidant molecules on reducing oxidative damage have been investigated in most of these studies. [3][4][5][6][7][8][9][10][11] It has been demonstrated that oxidative damage can be partially reduced by these drugs. However, there are as yet no molecules approved as an effective method to prevent AG nephropathy in clinical practice.…”

The impact of alpha-lipoic acid on amikacin-induced nephrotoxicity

“…22,36 Histopathological studies strongly support the concept that tubular necrosis is the primary cause of functional toxicity. 5,30,35 In this study, biochemical findings were confirmed by histopathological observation. The AK-applied group showed the highest lesions scores of glomerular congestion, mononuclear cell infiltration, tubular dilatation, cortical and medullary hemorrhage, proximal and distal tubular degeneration, which indicate renal tissue damage.…”

“…The evidence of AK-induced renal damage was demonstrated in several experiments with oxidative stress mechanism in rats. 4,5,13,14,21 ALA is widely used as a therapeutic agent for the treatment or prevention of diabetes complications, including polyneuropathy, cataract and nephropathies. [22][23][24] Nowadays, in several studies, antioxidant properties of ALA have been working mainly.…”

“…Recent studies demonstrate that reactive oxygen species have a role in the pathogenesis of AK nephrotoxicity. 4,5 Alpha-lipoic acid (ALA) is a naturally occurring dithiol compound that functions as an essential cofactor for mitochondrial enzymes. 6 When applied regularly, ALA accumulates in tissues and is converted to dihydrolipoic acid (DHLA) by lipoamide dehydrogenase.…”