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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
Author(s) -
Erdélyi M.,
Balogh K.,
Pelyhe C.,
Kövesi B.,
Nakade M.,
Zándoki E.,
Mézes M.,
Kovács B.
Publication year - 2018
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/jpn.12896
Subject(s) - aflatoxin , glutathione , glutathione reductase , lipid peroxidation , malondialdehyde , glutathione peroxidase , chemistry , antioxidant , peroxidase , endocrinology , medicine , biochemistry , biology , food science , enzyme
Summary The purpose of this study was to investigate the short‐term (48 hr) effects of feeding aflatoxin contaminated diet (170.3 μg/kg AFB 1) 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, conjugated dienes and trienes did not change as effect of aflatoxin, but terminal marker, malondialdehyde content was significantly higher at 12 hr as effect of aflatoxin. No significant difference was found in reduced glutathione concentration and glutathione peroxidase activity between the groups. Expression of glutathione peroxidase 4 gene ( GPX 4) was significantly reduced due to aflatoxin treatment at 12 and 24 hr, but induced later, while glutathione reductase gene ( GSR ) expression was significantly lower at 24 hr and glutathione synthetase gene ( GSS ) in aflatoxin‐treated group at 12 hr. The results suggest that aflatoxin induced oxygen‐free radical formation, but it did not reach critical level during this short period of time to cause activation of the expression of glutathione system.