Retinol, ascorbic acid and α-tocopherol prevent DNA adduct formation in mice treated with the mycotoxins ochratoxin A and zearalenone

Grosse, Yann; Chekir‐Ghedira, Leila; Huc, A.; Obrecht-Pflumio, Sophie; Dirheimer, G.; Bacha, Hassen; Pfohl‐Leszkowicz, Annie

doi:10.1016/s0304-3835(97)04669-7

Cited by 125 publications

(64 citation statements)

References 14 publications

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“…However, the protection of -SH groups/GSH by vitamin A as evident from the stated data could be due to its ability to scavenge the oxygen radicals consequently preventing the free radical attack. Grosse et al 40) have indicated vitamin A as an efficient •O 2 -scavenger; infact the antioxidant action of carotenoids are based on their singlet oxygen quenching property, which is also its best-documented action. 41) Several studies have also reported vitamin A to be an effective lipid antioxidant.…”

Section: Discussionmentioning

confidence: 99%

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Amelioration by Vitamin A upon Arsenic Induced Metabolic and Neurotoxic Effects

Gopalkrishnan

Rao

2006

JOURNAL OF HEALTH SCIENCE

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Arsenic effect was studied at two dosage levels (0.5 mg and 1 mg/kg) for 45 days in two regions of brain, viz., cerebral hemisphere (CH) and cerebellum (C) in adult mice. This study included the antioxidant profile namely superoxide dismutase (SOD), catalase, lipid peroxidation, reduced glutathione, ascorbic acid and total sulphydryl groups. Adenosine triphosphatase (ATPase), succinic dehydrogenase (SDH), phosphorylase together with glycogen and protein levels were also estimated as metabolic indices in the brain regions of mice. A notable decrease was detected in the activities of the enzymes and in the levels of other metabolites together with a significant increase in the lipid peroxidation, glycogen and inorganic arsenic levels after arsenic administration. Supplementation of vitamin A to the arsenic treated mice brought about no significant variation in these antioxidant and metabolic indices in comparison to that of control, revealing amelioration by vitamin A on arsenic exerted metabolic and neurotoxic effects in mice.Key words ---arsenic, vitamin A, antioxidant system, metabolic and neurotoxic effect in part by inducing rapid burst of reactive oxygen species (ROS) in mammalian cells, resulting in oxidative stress 12,13) and carcinogenesis in man. 14) Studies document that arsenic generates ROS such as hydrogen peroxide, superoxide (O 2•-), hydroxyl (OH • ) and peroxyl (ROO • ) radicals. 13) These free radicals and the other reactive species are constantly produced in the brain in vivo.15) Experiments on human fetal brain explants on exposure to arsenic in culture have showed disturbances in lipid peroxidation, generation of ROS and apoptosis. 16) Adenosine triphosphatase (ATPase) and succinic dehydrogenase (SDH) (enzymes of the inner mitochondrial membrane) are concerned with respiration, and energy generation; hence, are essential for cell survival. Respiratory chain is the major source of ROS, hence mitochondrial oxidative damage is thought to be a proximal cause of metabolic effects. 17,18) Metabolism in fish brain was also affected by arsenic poisoning 19) in addition to other pathological effects in general metabolism of animal tissues. 20)

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Section: Discussionmentioning

confidence: 99%

“…These results indicate that vitamin A may act as a physiological antioxidant in cell membranes where it is localized. 53) Grosse et al 40) have indicated vitamin A as an efficient •O 2 -scavenger; infact the antioxidant action of vitamin A is based on their singlet oxygen quenching property, which is also its best documented action.…”

Section: Discussionmentioning

confidence: 99%

Amelioration by Vitamin A upon Arsenic Induced Metabolic and Neurotoxic Effects

Gopalkrishnan

Rao

2006

JOURNAL OF HEALTH SCIENCE

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“…Antioxidants were shown to prevent OTA-mediated increases in MDA production in vitro (Baudrimont et al 1997) and in vivo (Meki and Hussein 2001). In rats, the injection of superoxide dismutase and catalase provided protection against OTA-induced nephrotoxicity in vivo (Baudrimont et al 1994), and in mice, antioxidant vitamins reduced an OTAmediated increase in chromosomal aberrations (Manolova et al 1990) and the formation of 32 P-postlabelling spots (Grosse et al 1997). Several potential relevant oxido-reduction mechanisms have been identified and proposed.…”

Section: Oxidative Stressmentioning

confidence: 99%

Ochratoxin A: Potential epigenetic mechanisms of toxicity and carcinogenicity

Schilter

Marin-Kuan

Delatour

et al. 2005

Food Additives & Contaminants

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Assessment of the significance to human health of ochratoxin A (OTA) in food is limited by a lack of human toxicity data. Therefore, OTA risk evaluation relies mainly on the use of animal data, with renal carcinogenicity in rat being considered as the pivotal effect. The elucidation of the mechanism of action would improve the use of the carcinogenicity data for risk assessment. Direct genotoxicity versus epigenetic mechanisms appears to be a key question. In this presentation, new biochemical and toxicogenomic results obtained in a recent European project (EU-Grant # QLK1-CT-2001-011614) will be summarized in the context of previously reported mechanisms of action including inhibition of protein synthesis, production of oxidative stress and alteration of cell signalling. Amongst others, the new data indicate that chronic administration of a carcinogenic dose of OTA affected cell-signalling pathways resulting in a significantly reduced renal antioxidant defence and increased oxidative DNA damage. These data confirm previous hypotheses involving oxidative stress as a possible key epigenetic mechanism of OTA toxicity and carcinogenicity.

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“…Nip et al 80 reported that OTA in barley passed into beer with a 14-18% reduction and Chu et al 31 found that the OTA in barley decreased 14-28% when used in beer production and 70% of the OTA was degraded in the production steps 50 . Gjerten et al 47 noted that the OTA in the malt passes to the beer with a 10% reduction.…”

Section: Ochratoxin a Changes During Brewingmentioning

confidence: 99%

“…These properties are probably due to the ability that the antioxidants have to act as superoxide anion scavengers, thereby protecting the cell membrane from mycotoxin-induced damage and they have protective effects against the toxic action 7,13 of OTA. In vitro and in vivo studies show that melatonin 2 , rosmarinic acid 93 , α-tocopherol, retinol, cyanidin-3-o-bglucopyranoside 50 , ascorbic acid 49 , L-methionine 1 , aspartame 34 , polyphenols 32 , combined antioxidants 12 and different alkaloids 65 counteract some of the toxic effects 7 of OTA.…”

Section: Detoxification Of Ochratoxin Amentioning

confidence: 99%

Ochratoxin A and Brewing Technology: A Review

Anlı

Alkış

2010

Journal of the Institute of Brewing

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Ochratoxins are a hazardous group of mycotoxins produced as secondary metabolites by several fungi of the Aspergillus and Penicillium families. Ochratoxins have been detected and determined in foods and beverages, including barley, malt and beer, at ppb levels. Varied analytical methods have been developed for the detection of ochratoxin A [OTA] in cereals and beer. Ochratoxin A has hazardous effects on health and has been classified within group 2B, as a possible human carcinogen by IARC. Scientists have expressed great concern about the presence of ochratoxin A in foods. In this article, chemical structure, biosynthesis by microorganisms, analytical methods for testing, regulations, changes during brewing, and detoxification of OTA, are reviewed. Beer poses very little risk as a source of ochratoxin in the diet.

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Retinol, ascorbic acid and α-tocopherol prevent DNA adduct formation in mice treated with the mycotoxins ochratoxin A and zearalenone

Cited by 125 publications

References 14 publications

Amelioration by Vitamin A upon Arsenic Induced Metabolic and Neurotoxic Effects

Amelioration by Vitamin A upon Arsenic Induced Metabolic and Neurotoxic Effects

Ochratoxin A: Potential epigenetic mechanisms of toxicity and carcinogenicity

Ochratoxin A and Brewing Technology: A Review

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