2018
DOI: 10.1111/jpn.12896
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Changes in the regulation and activity of glutathione redox system, and lipid peroxidation processes in short‐term aflatoxin B1 exposure in liver of laying hens

Abstract: The purpose of this study was to investigate the short-term (48 hr) effects of feeding aflatoxin contaminated diet (170.3 μg/kg AFB1) in 49-week-old laying hens. Liver samples were taken at 12-hr intervals. Feed intake, body weight, absolute and relative liver weight were the same in groups. However, there was no feed intake during both dark periods (between 12nd to 24th and 36th to 48th hours of the experiment); therefore, aflatoxin intake was also negligible. Markers of initial phase of lipid peroxidation, c… Show more

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Cited by 13 publications
(9 citation statements)
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“…It seems likely that dysregulation of the antioxidant defense network and disruption of redox balance and signaling are important steps in mycotoxin-related stresses. This is true not only for OTA (this paper), but also for T-2 toxin [14], aflatoxins [15] and other mycotoxin exposure singly or in combination [16]. Therefore, elucidation of molecular mechanisms of dysregulating actions of mycotoxins on the antioxidant defense network and search for an effective strategy to deal with mycotoxin-related nutritional stresses in poultry production warrants further research.…”
mentioning
confidence: 84%
“…It seems likely that dysregulation of the antioxidant defense network and disruption of redox balance and signaling are important steps in mycotoxin-related stresses. This is true not only for OTA (this paper), but also for T-2 toxin [14], aflatoxins [15] and other mycotoxin exposure singly or in combination [16]. Therefore, elucidation of molecular mechanisms of dysregulating actions of mycotoxins on the antioxidant defense network and search for an effective strategy to deal with mycotoxin-related nutritional stresses in poultry production warrants further research.…”
mentioning
confidence: 84%
“…This finding is consistent with the increased content of a series of lipid peroxidation products in AFs-treated hepatocytes, e.g., conjugated dienes, lipid hydroperoxides and malonaldehyde (MDA). And MDA, a terminal marker of lipid peroxidation, is an important factor that reflects alteration of membrane fluidity ( Gesing and Karbownik-Lewinska, 2008 ; Shi et al, 2012b ; Ajiboye et al, 2016 ; Erdélyi et al, 2018 ). Protein oxidation or carbonylation are important oxidative steps of toxicities in mitochondria.…”
Section: Afs Damage Mitochondria To Initiate Various Cellular Injury mentioning
confidence: 99%
“…Moreover, most of the conducted research reported that the toxicity of AFB1 in Caco-2 and HepG2 cells occurs at a dose of 3.0 µg/mL [29,30]. AFB1 has been found to induce oxidative radical formation through the cytochrome-activated P450 enzyme system, generating lipid peroxidation and reducing antioxidant enzyme activity [31], resulting in the carcinogenicity. These radicals may induce pathologies by damaging lipids, proteins and DNA [32].…”
Section: Introductionmentioning
confidence: 99%