Effect of chronic exposure to sublethal of ammonia concentrations on NADP+-dependent dehydrogenases of Nile tilapia liver

Abstract

he effect of chronic exposure to sublethal ammonia (NH 3) on liver NADPH producing enzymes of Nile tilapia juveniles (Oreochromis niloticus) was studied. Fish with an initial weight of 15.0±1.4 g were reared in a static system and exposed to the total ammonia nitrogen (TAN) concentrations 5 or 10 mg L −1 for consecutive 70 days at 26±0.5°C. NADPH is mainly produced by glucose 6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and the cytosolic form of NADP-dependent isocitrate dehydrogenase (IDH). These enzymes have been recently considered as an important factor in cellular defense against oxidative damage as they share in maintaining reduced glutathione (GSH) level. The activity of the enzymes G6PDH, 6PGDH, and cytosolic IDH in liver tissues of fish exposed to different concentrations of NH 3 showed significant increase. The degree of increase in activity was positively related to ammonia concentration. The increased activity of these enzymes resulted in higher NADPH availability. This may be interpreted as a defense to maintain a high level of GSH against the expected oxidative stress in ammonia-exposed fish.

Oxidative Stress and Antioxidant Defense to Acute Changes of Water Ph in Liver and Muscle of Three Ornamental Fish

“…Bagnyukova et al, (2006) reports also showed increased levels of lipid peroxidation products (TBARS and LOOH) in gold sh liver exposed to pH shift due to addition of limestone water in rearing tanks. Similar increases in lipid peroxidation were recorded in response to ammonia exposure in Nile tilapia and silver carp by Sun et al (2011) and Hegazi (2011) respectively. Occurrence of oxidative stress can be assessed by changes in levels of oxidative damage markers as products of protein and lipid peroxidation (Storey, 1996;Hermes-Lima, 2004).…”

Anti-Oxidative Defences Are Modulated Differentially in Three Freshwater Teleosts in Response to Ammonia-Induced Oxidative Stress

“…Malondialdehyde (MDA), the oxidative end product of PUFAs increased in both trout and cyprinid liver under ammonia stress. Increases in lipid peroxidation in response to ammonia exposure have been reported for Nile tilapia [31] , [66] , mudskipper ( Boleophthalmus boddarti ) [30] , bighead carp ( Hypophthalmythys nobilis ) [32] and silver carp ( Hypophthalmichthys molitrix ) [65] . Furthermore, similar to the H 2 O 2 response, elevated MDA levels in trout persisted longer and failed to re-establish to control levels in contrast to MDA levels in cyprinids.…”

High environmental ammonia elicits differential oxidative stress and antioxidant responses in five different organs of a model estuarine teleost ( Dicentrarchus labrax )

“…The parallel augmentations of GR with GPX activity in liver tissue justify a proficient renewal of GSH. It is reported that GSH synthesis can be immensely triggered as a consequence of ammonia pollution, observed in the liver of several ammonia-exposed fish (Hegazi, 2011;Sinha et al, 2014b). Liver is also the main storage site for GSH prior to transportation to other organs via blood, and this metabolite is anticipated to provide extraordinary resilience to hepatic cell against oxidative damage (Winzer et al, 2002).…”

“…These include-minimize the ammonia production by suppression of amino acid catabolism, conversion of accumulated ammonia into free amino acids particularly glutamine, detoxification of ammonia to the less toxic urea, and augmentation of ammonia excretion by up-regulation of 'Na +/ NH 4 + exchange complex' involving the Rh glycoproteins (Wright and Wood, 2009). Furthermore, some studies suggest that ammonia exerts the (cyto)toxic effects in fish by the production of reactive oxygen species (ROS) such as superoxide (O 2 2010;Hegazi, 2011;Sun et al, 2011Sun et al, , 2012Sinha et al, 2014b). ROS are generated as by-products of oxidative metabolism, and high production and accumulation of ROS could result in build-up of oxidized and damaged lipids and proteins in the cellular compartments, eventually inducing oxidative damage (Droge, 2003).…”