| Literature DB >> 26073360 |
Amit Kumar Sinha1, Gaurav Zinta2, Hamada AbdElgawad3, Han Asard2, Ronny Blust4, Gudrun De Boeck4.
Abstract
We investigated oxidative status and antioxidant profile in five tissues (brain, liver, gills, muscle and kidney) of European sea bass (Dicentrarchus labrax) when exposed to high environmental ammonia (HEA, 20 mg/L~1.18 mM as NH4HCO3) for 12 h, 2 days, 3.5 days, 7.5 days and 10 days. Results show that HEA triggered ammonia accumulation and induced oxidative stress in all tissues. Unlike other organs, hydrogen peroxide (H2O2) and malondialdehyde (MDA) accumulation in liver were restored to control levels. This recovery was associated with a concomitant augmentation in superoxide dismutase (SOD), catalase (CAT), components of glutathione redox cycle (glutathione peroxidase GPX, glutathione reductase, reduced glutathione), ascorbate peroxidase activity and reduced ascorbate content. On the contrary, in brain during prolonged exposure many of these anti-oxidant enzymes were either unaffected or inhibited, which resulted in persistent over-accumulation of H2O2 and MDA. Branchial and renal tissue both involved in osmo-regulation, revealed an entirely dissimilar compensatory response; the former rely mainly on the ascorbate dependent defensive system while the glutathione catalytic pathway was activated in the latter. In muscle, GPX activity first rose (3.5 days) followed by a subsequent drop, counterbalanced by simultaneous increment of CAT. HEA resulted in a relatively mild oxidative stress in the muscle and kidney, probably explaining the modest anti-oxidative responses. Our findings exemplify that oxidative stress as well as antioxidant potential are qualitatively diverse amongst different tissues, thereby demonstrating that for biomonitoring studies the screening of adaptive responses at organ level should be preferred over whole body response.Entities:
Keywords: Antioxidant defense system; Brain; European sea bass; Gills; Hydrogen peroxide (H(2)O(2)); Liver; Malondialdehyde (MDA)
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Year: 2015 PMID: 26073360 DOI: 10.1016/j.cbpc.2015.06.002
Source DB: PubMed Journal: Comp Biochem Physiol C Toxicol Pharmacol ISSN: 1532-0456 Impact factor: 3.228