Quercetin protects human peripheral blood mononuclear cells from OTA‐induced oxidative stress, genotoxicity, and inflammation

Abstract

Ochratoxin A (OTA) is one of the most abundant food-contaminating mycotoxins world wide, and is detrimental to human and animal health. This study evaluated the protective effect of quercetin against OTA-induced cytotoxicity, genotoxicity, and inflammatory response in lymphocytes. Cytotoxicity determined by MTT assay revealed IC20 value of OTA to be 20 µM, which was restored to near control values by pretreatment with quercetin. Oxidative stress parameters such as antioxidant enzymes, LPO and PCC levels indicated that quercetin exerted a protective effect on OTA-induced oxidative stress. Quercetin exerted an antigenotoxic effect on OTA-induced genotoxicity, by significantly reducing the number of structural aberrations in chromosomes and comet parameters like, % olive tail moment from 2.76 ± 0.02 to 0.56 ± 0.02 and % tail DNA from 56.23 ± 2.56 to 12.36 ± 0.56 as determined by comet assay. OTA-induced NO, TNF-α, IL-6, and IL-8 were significantly reduced in the quercetin pretreated samples indicating its anti-inflammatory role. Our results demonstrate for the first time that quercetin exerts a cytoprotective effect against OTA-induced oxidative stress, genotoxicity, and inflammation in lymphocytes. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 855-865, 2016.

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

“…However, the exact mechanism of OTA‐induced nephrotoxicity has not yet been completely understood. The results obtained in this study, in accordance with in vitro and in vivo studies (Abdel‐Wahhab, Aljawish, El‐Nekeety, Abdel‐Aziem, & Hassan, ; Ciarcia et al, ; Costa et al, ; Periasamy, Kalal, Krishnaswamy, & Viswanadha, ), confirmed that the toxic effect of OTA on the kidney found both on the functional level and from the histopathology of view is mediated by oxidative stress. It has been shown that OTA acts by inhibiting the nuclear factor, which would affect both the synthesis and the recycling of glutathione and also the activity of oxidoreductases thus making the tissue more vulnerable to oxidative stress (Jennings, Limonciel, Felice, & Leonard, ; Limonciel & Jennings, ).…”

Effects of Curcumin on the Renal Toxicity Induced by Ochratoxin A in Rats

“…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.…”

“…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 Significance of Regulatory MicroRNAs: Their Roles in Toxicodynamics of Mycotoxins and in the Protection Offered by Dietary Therapeutics Against Mycotoxin‐Induced Toxicity

“…Many studies indicated that quercetin could ameliorate OTA‐induced oxidative stress in different types of cells such as human peripheral blood mononuclear cells, HepG2 cells, and Vero cells, and the Nrf2 pathway might play essential roles in the regulation of quercetin on Vero cell line (Periasamy, Kalal, Krishnaswamy, & Viswanadha, ; Ramyaa & Padma, ; Ramyaa, Krishnaswamy, & Padma, ). Similarly, quercetin at 5 μM was found to offer a protective effect against the cellular toxicity of α‐ZOL (180 μM) or β‐ZOL (300 μM), through inhibiting oxidative stress, endoplasmic reticulum stress and cell apoptosis via a mitochondria‐dependent pathway (Ben Salem, Prola et al., ).…”