Adapted response of the antioxidant defense system to oxidative stress induced by deoxynivalenol in Hek-293 cells

Dinu, Diana; Bodea, Gabriela O.; Ceapă, Corina Diana; Munteanu, Maria Cristina; Roming, Florentina Israel; Serban, Andreea Iren; Hermenean, Anca; Costache, Marieta; Zarnescu, Otilia; Dinischiotu, Anca

doi:10.1016/j.toxicon.2011.04.006

Cited by 47 publications

(22 citation statements)

References 42 publications

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“…This finding suggests that GSH is involved in the cellular defense mechanisms in response to the exposure to this mycotoxin in Caco-2 cells. Similar results were obtained by Tiessen et al (2013) who showed that GSH levels decreased (from 19% to 26%) in a concentration dependent manner in HT29 cells after exposure to 10-50 mM AOH for 1 h. Furthermore, parallel results were observed with mycotoxins from other genera of fungi (Penicillium,Aspergillus and Fusarium), like deoxynivalenol (DON) in human peripheral blood lymphocytes (PBL) (Yang et al, 2014) and Hek-293 (Dinu et al, 2011); Beauvericin (BEA) in Caco-2 cells (Prosperini et al, 2013) and CHO-K1 cells (Mallebrera et al, 2014); Zearalenone (ZEA) in HepG2 cells (Hassen et al, 2007); Ochratoxin (OTA) in LLC-PK1 cells (Schaaf et al, 2002) and T-2 toxin in GPCS cells (He et al, 2011).…”

Section: Discussionsupporting

confidence: 81%

Oxidative DNA damage and disturbance of antioxidant capacity by alternariol in Caco-2 cells

2015

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Section: Discussionsupporting

confidence: 81%

Oxidative DNA damage and disturbance of antioxidant capacity by alternariol in Caco-2 cells

2015

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“…These results are contrary to those obtained in vitro with mouse colon cells, in which DON increased SOD activity in association with increased production of ROS (Krishnaswamy et al 2010). SOD and GPx work in tandem, SOD decomposing ROS by converting them to hydrogen peroxide, which is decomposed by CAT and GPx (Dinu et al 2011). In the present study, the increased GPx activity in the ileum may be due to overproduction of ROS.…”

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confidence: 99%

“…(P B0.05) Finally, none of the experimental treatments had any effect on the MDA concentration in ileum or on TAC in the ileum or jejunum. The adverse effects of DON on intestinal tissue may be due to increased production of free radicals and reactive oxygen species (ROS), resulting in oxidative damage to enterocytes (Kouadio et al 2005;Dinu et al 2011;Li et al 2014). DON-induced overproduction of ROS has been shown in vitro to cause oxidative injury, including DNA damage, protein oxidation and lipid peroxidation in cells (Mates 2000).…”

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confidence: 99%

“…Serum CAT activity was decreased in pigs fed a diet containing about 4 mg kg (1 (Xiao et al 2013), the same amount that affected this enzyme in the piglet jejunum presently. An in vitro study conducted using kidney cells showed that CAT activity was up-regulated at low concentrations of DON, but down-regulated at high concentrations (Dinu et al 2011). The reduction in CAT activity may be due to accumulation of superoxide anions (O 2( ), which are inhibitory (Kono and Fridovich 1982).…”

mentioning

confidence: 99%

“…Despite the lack of effect on MDA concentration in the ileum, SOD activity was decreased while GPx activity was increased. Indeed, SOD represents the first line of antioxidant defence, followed by CAT and GPx, which can be activated to remove free-radical superoxides (Dinu et al 2011). A previous study found a reduction in SOD activity in the serum of pigs fed a diet containing DON at about 4 mg kg…”

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confidence: 99%

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Short Communication: Antioxidant capacity in the intestinal mucosa of weanling piglets fed diets containingFusariummycotoxins and the efficacy of commercial supplements sold as detoxifiers

et al. 2015

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Le Thanh, B. V., Lessard, M., Chorfi, Y. and Guay, F. 2015. Short Communication: Antioxidant capacity in the intestinal mucosa of weanling piglets fed diets containing Fusarium mycotoxins and the efficacy of commercial supplements sold as detoxifiers. Can. J. Anim. Sci. 95: 569–575. The ability of commercial feed additives to prevent oxidative damage due to deoxynivalenol (DON) in piglets was studied. Sixty piglets (6.0±0.5 kg) were assigned randomly to six wheat–corn–soybean diets: control (<0.5 mg kg−1 DON), DON-rich diet (4 mg kg−1 DON), and four DON-rich diets supplemented with either glucomannan (DON+GLUC), yeast, live bacteria, enzymes and plant extract (DON+YBP), aluminosilicate (DON+ALS), or a mixture of preservatives (DON+PV). Malondialdehyde concentration (MDA), glutathione peroxidase activity (GPx), catalase activity (CAT) and superoxide dismutase activity (SOD) in the small intestine were measured after 14 d. The DON-rich diet increased MDA in the jejunum while decreasing CAT in the jejunum and SOD in the ileum and increasing GPx in the ileum (P<0.05). The DON+GLUC diet decreased GPx and SOD (P<0.05) and tended to decrease MDA in the jejunum (P<0.10). The DON+YBP, DON+PV and DON+ALS diets all decreased CAT in the jejunum, while DON+YBP and DON+PV also did so in the ileum (P<0.05). DON+GLUC decreased SOD in the jejunum, while DON+YBP increased it (P<0.05). In the ileum, DON+PV decreased SOD, while DON+ALS increased GPx (P<0.05). No significant differences in total antioxidant capacity (TAC) in intestinal tissues were found. This study demonstrates that the mycotoxin DON and anti-mycotoxin additives modify oxidative status, including the antioxidant enzyme activities (CAT, SOD or GPx) in the intestinal mucosa of piglets. However, it was not possible to identify a specific antioxidant enzyme involved in counteracting the effect of DON.

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Toxicology of deoxynivalenol and its acetylated and modified forms

et al. 2016

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Mycotoxins are the most frequently occurring natural contaminants in human and animal diet. Among them, deoxynivalenol (DON), produced by Fusarium, is one of the most prevalent and thus represents an important health risk. Recent detection methods revealed new mycotoxins and new molecules derivated from the "native" mycotoxins. The main derivates of DON are the acetylated forms produced by the fungi (3- and 15-acetyl-DON), the biologically "modified" forms produced by the plant (deoxynivalenol-3-β-D-glucopyranoside), or after bacteria transformation (de-epoxy DON, 3-epi-DON and 3-keto-DON) as well as the chemically "modified" forms (norDON A-C and DON-sulfonates). High proportions of acetylated and modified forms of DON co-occur with DON, increasing the exposure and the health risk. DON and its acetylated and modified forms are rapidly absorbed following ingestion. At the molecular level, DON binds to the ribosome, induces a ribotoxic stress leading to the activation of MAP kinases, cellular cell-cycle arrest and apoptosis. The toxic effects of DON include emesis and anorexia, alteration of intestinal and immune functions, reduced absorption of the nutrients as well as increased susceptibility to infection and chronic diseases. In contrast to DON, very little information exists concerning the acetylated and modified forms; some can be converted back to DON, their ability to bind to the ribosome and to induce cellular effects varies according to the toxin. Except for the acetylated forms, their toxicity and impact on human and animal health are poorly documented.

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Adapted response of the antioxidant defense system to oxidative stress induced by deoxynivalenol in Hek-293 cells

Cited by 47 publications

References 42 publications

Oxidative DNA damage and disturbance of antioxidant capacity by alternariol in Caco-2 cells

Oxidative DNA damage and disturbance of antioxidant capacity by alternariol in Caco-2 cells

Short Communication: Antioxidant capacity in the intestinal mucosa of weanling piglets fed diets containingFusariummycotoxins and the efficacy of commercial supplements sold as detoxifiers

Toxicology of deoxynivalenol and its acetylated and modified forms

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