Effect of Ethanol and Red Wine on Ochratoxin A-Induced Experimental Acute Nephrotoxicity

Abstract

Ochratoxin A (OTA), is a nephrotoxic mycotoxin present in wine, which is nephrotoxic in humans. Our working hypothesis is that natural substances in wine may counteract OTA toxicity. Thirty-six rats were randomized to OTA dissolved in saline, red wine, or 13.5% ethanol or to OTA-free wine, ethanol, or saline. OTA (289 microg/kg of body weight/48 h) was administered by gastric gavage for 2 weeks. Serum creatinine, tubular enzymuria, renal lipohydroperoxides (LOOH), reduced (GSH) and oxidized (GSSG) glutathione, and renal superoxide dismutase activity (SOD) were determined in renal tissue. OTA alone produced significant increases in renal lipoperoxides and significant decreases in SOD and GSH/GSSG ratio. In red wine or ethanol, OTA was less nephrotoxic, reducing oxidative damage as revealed by LOOH. In OTA-wine and OTA-ethanol groups, SOD activity was higher than in the OTA-treated one, suggesting that both ethanol and nonalcoholic fractions may preserve antioxidant reserve. GSH/GSSG ratio was significantly preserved only in the OTA-wine group and not in OTA-ethanol. Red wine may exert a protective effect against OTA nephrotoxicity by limiting oxidative damage. The ostensible protection afforded by ethanol deserves further investigation.

Red orange and lemon extract prevents the renal toxicity induced by ochratoxin A in rats

“…These data, according to our previous works (Damiano et al, , ) and to Palabiyik et al () and Domijan et al () suggest that the restoring potential of RLE on OTA nephrotoxicity is related to its direct scavenging in activity on ROS, rather than its modulation of cellular enzymatic activities. It is interesting to note, in this study, in line with the study conducted by Bertelli et al (), the GSH enzymatic activity in OTA group was reduced compared to the control group instead of in the OTA and RLE group the GSH levels returned to baseline values. This data is probably because OTA is transforming into a more toxic species, OTQ 6, that would provide a basis for the toxins’ ability to promote oxidative stress (Dai et al, ).…”

Ochratoxin A induces apoptosis in neuronal cells

“…In vitro and in vivo data suggest an involvement of oxidative stress in OTA-mediated cytotoxicity [1,4,16,17,23,30]. In fact, we observed in kidney tubulus cells a significant increase in reactive oxygen species production after OTA treatment already at relatively low OTA concentrations (0.5-2.5 lmol/L) [5] which were similar to those concentrations we used in the present study in neurons.…”

Facilitation of central imidazoline I1‐site/extracellular signal‐regulated kinase/p38 mitogen‐activated protein kinase signalling mediates the hypotensive effect of ethanol in rats with acute renal failure

“…(2004) demonstrated that whereas chronic exposure to ethanol does not alter renal derangements caused by glycerol, it reinforces the renoprotective effect of polyphenolic compounds of alcohol‐free red wine. Likewise, ethanol exerts a protective effect against nephrotoxicity induced by ochratoxin (Bertelli et al. , 2005).…”

“…The up‐regulation of the activity of antioxidant enzymes probably mediates the beneficial effect of ethanol (Rodrigo et al. , 2004; Bertelli et al. , 2005).…”