# Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats
## 4 Discussion  
OTA is a well-known and widely spread mycotoxin all over the world, which exerts dangerous effects on human and animal health [28]. Therefore, it is crucial to examine the toxic effects of OTA and to protect from its damage. The kidney is one of the most vulnerable target organs of OTA-induced toxicity [29]. Despite the numerous strategies developed to reduce OTA-induced nephrotoxicity, this mycotoxin mechanism of action remains complex and unknown. However, in recent years, several in vivo and in vitro studies have recognized that the induction of the oxidative stress induced by OTA exposure is considered one of the mechanisms responsible for its toxicity [30; 31; 32; 33]. Thus, the administration of antioxidants that counteract oxidative stress may protect kidneys from damage. Nephrotoxicity studies have confirmed the authentic roles of bioactive compounds to reduce chronic renal failure [27; 34; 35; 36]. The present study investigated CURC effects on OTA-induced toxicity using an in vivo animal model. CURC is a polyphenolic diketone natural product, commonly known as turmeric, with a multiplicity of pharmacologic properties. CURC is known to exert anti-inflammatory and antioxidant effects in various pathologies [37]. However, the protective effects of curcumin against OTA-mediated nephrotoxicity have not yet been studied using a mouse model. Therefore, the aim of our study was to examine the protective effects of CURC on OTA-induced renal toxicity through the evaluation of renal function and its main antioxidant enzymatic activities. To increase the stability and intestinal absorption of CURC, we used corn oil as a solvent. Due to good intestinal absorption, CURC increased the body weights of rats intoxated by OTA after 14 days of treatment and, therefore, demonstrated a protective effect on the body weight of rats, considering that body weight is a main indicator for the assessment of toxic impacts of various drugs or chemicals on animals [38]. Actually, in our previous works carried out on rats treated with OTA we have always found a significant decrease in body weight compared to the control group subjects, as index of toxicity [7; 27]. It is well-known that oxidative stress occurs due to an imbalance between oxidant and antioxidant systems, which could be due to elevated free radical generation and decreased antioxidant activity. Several studies suggest that both in vitro and in vivo OTA exposure results in the overproduction of free radicals [22; 32; 33], causing damage to cell constituents such as membrane lipids. Therefore, the main antioxidant enzymes, such as CAT, SOD and GPx, play a crucial role in protection against oxidative stress [39]. The results obtained in this study, in accordance with our previous works [7; 21; 27], confirmed that the renal toxic effects of OTA, both on a functional and histopathological level, is mediated by oxidative stress. Actually, in this study we found an increase of MDA in the kidneys of rats treated with OTA, which is an index of membrane lipid damage, and a decrease mainly in the activity of GPx, in line with the study conducted by [PERSON], et al. [40; 41]. Furthermore, this study, according to the studies of [PERSON] et al. [42] and [PERSON] et al. [43], allows us to hypothesize that the toxic action of OTA is partly linked to its modulation on enzymatic activities and partly to a direct action on the production of ROS. CURC has been documented as a good antioxidant agent by many researchers [44; 45; 46] and the use of antioxidants has been shown to reduce oxidative stress either by eliminating free radicals or by rectifying the activity of the antioxidant defense system [47]. Here, CURC significantly reduced values of the lipid peroxidation with a consequent attenuation of the adverse effects of the chronic stress induced by OTA on tissue damage.