Effects of salinity stress on antioxidant status and inflammatory responses in females of a "Near Threatened" economically important fish species Notopterus chitala: a mechanistic approach.

In the present study, acute stress responses of adult female Notopterus chitala were scrutinized by antioxidant status and inflammation reaction in the gill and liver at five different salinity exposures (0, 3, 6, 9, 12 ppt). Oxidative defense was assessed by determining superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase, and glutathione reductase activities, while malondialdehyde (MDA), glutathione, and xanthine oxidase levels were determined as indicators of oxidative load. Pro-inflammatory cytokines (IL-1ß, IL-6, IL-10, and TNFα) and caspase 1 levels were also analyzed. Expression levels of transcription factors (NRF2 and NF-κB) and molecular chaperons (HSF, HSP70, and HSP90) were estimated to evaluate their relative contribution to overcome salinity stress. MDA showed a significant (P < 0.05) increase (gill, + 25.35-90.14%; liver, + 23.88-80.59%) with salinity; SOD (+ 13.72-45.09%) and CAT (+ 12.73-33.96%) exhibited a sharp increase until 9 ppt, followed by a decrease at the highest salinity (12 ppt) (gill, - 3.92%; liver, - 2.18%). Levels of cytokines were observed to increase (+ 52.8-127.42%) in a parallel pattern with increased salinity. HSP70 and HSP90 expressions were higher in gill tissues than those in liver tissues. NRF2 played pivotal role in reducing salinity-induced oxidative load in both the liver and gills. Serum cortisol and carbonic anhydrase were measured and noted to be significantly (P < 0.05) upregulated in salinity stressed groups. Gill Na+-K+-ATPase activity decreased significantly (P < 0.05) in fish exposed to 6, 9, and 12 ppt compared to control. Present study suggests that a hyperosmotic environment induces acute oxidative stress and inflammation, which in turn causes cellular death and impairs tissue functions in freshwater fish species such as Notopterus chitala.

Physiological response of fish under variable acidic conditions: a molecular approach through the assessment of an eco-physiological marker in the brain.

The current study demonstrates oxidative damage and associated neurotoxicity following pH stress in two freshwater carp Labeo rohita and Cirrhinus cirrhosus. Carp (n = 6, 3 replicates) were exposed to four different pH (5.5, 6, 7.5, and 8) against control (pH 6.8 ± 0.05) for 7 days. After completion of treatment, levels of enzymatic (superoxide dismutase [SOD], catalase [CAT], glutathione reductase [GRd]) and non-enzymatic antioxidants (malondialdehyde [MDA], glutathione [GSH]), brain neurological parameters (Na+-K+ATPase, acetylcholinesterase [AcHE], monoamine oxidase [MAO], and nitric oxide [NO]), xanthine oxidase (XO), heat shock proteins (HSP70 and HSP90), and transcription factor NFkB were measured in carp brain. Variation in the pH caused a significant alteration in the glutathione system (glutathione and glutathione reductase), SOD-CAT system, and stress marker malondialdehyde (MDA). Xanthine oxidase was also induced significantly after pH exposure. Brain neurological parameters (MAO, NO, AChE, and Na+-K+ATPase) were significantly reduced at each pH-treated carp group though inhibition was highest at lower acidic pH (5.5). Cirrhinus cirrhosus was more affected than that of Labeo rohita. Molecular chaperon HSP70 expression was induced in all pH-treated groups though such induction was more in acid-stressed fish. HSP90 was found to increase only in acid-stressed carp brain. Expression of NFkB was elevated significantly at each treatment group except for pH 7.5. Finally, both acidic and alkaline pH in the aquatic system was found to disturb oxidative balance in carp brain which ultimately affects the neurological activity in carp. However, acidic environment in the aquatic system was more detrimental than the alkaline system regarding oxidative damage and subsequent neurotoxicity in carp brain.