Suman Bhusan Chakraborty

The present study emphasizes the cAMP‐dependent signaling pathway, germinal vesicle breakdown (GVBD), and the role of the Nrf2–metallothionein (MT) system under metal‐induced oxidative stress. It compares how zinc (Zn) and lead (Pb) affect steroid‐driven oocyte maturation in the freshwater catfish Mystus vittatus via in vitro exposure of oocytes to inhibitory concentrations (1/10 IC₅₀: ZnSO₄ at 3.9 μM, Pb (NO₃) ₂ at 2.4 μM). Measurements included reactive oxygen species, Ca ²⁺ , cAMP‐protein kinase A, maturation‐inducing hormone (MIH), MT, estradiol receptor α, cyclin B–Cdc2, and the nuclear factor erythroid 2‐related factor 2 and Kelch‐like ECH‐associated protein 1 pathway. Exposure of oocytes to Zn and Pb significantly ( p < 0.05) reduced GVBD, MIH, and Ca ²⁺ levels, whereas estradiol and ERα remained unchanged. Pb exposure significantly ( p < 0.05) elevated cAMP and PKA. Cyclin B and Cdc2 protein levels significantly ( p < 0.05) dropped in metal‐exposed oocytes. Both metals significantly ( p < 0.05) increased ROS, with Pb inducing greater. MT and nuclear Nrf2 expression increased significantly ( p < 0.05), whereas cytosolic Keap1 significantly ( p < 0.05) declined, most markedly with Pb. Statistical analyses, including ANOVA, correlation, principal component analysis (PCA), and random forest model (RFM), were performed to understand the redox‐regulatory mechanisms of the oocyte maturation pathway in distinct, metal‐specific ways: Pb more strongly impaired steroid‐mediated oocyte maturation than Zn. PCA and RFM highlighted increased ROS, Nrf2, cAMP, and MT, with decreased MIH–MPF components, indicating that metal‐induced redox activation up‐regulated the Nrf2–MT pathway while suppressing maturation signals, thereby delaying oocyte maturation.

Present study aims to point out the antibacterial phytocomponents in Ceratophyllum demersum against Aeromonas sobria infection in Botia rostrata. In disc diffusion assay, C. demersum ethanol extract (CE) showed the highest antibacterial activity (17.66±0.33 mm). In subsequent in vivo study, healthy, juvenile B. rostrata males (Weight: 2.7±0.5 g; Length: 4.9±0.8 cm) were fed basal and CE-fortified (0.4 g/kg feed) diets for 30 days either before being intraperitoneally injected with A. sobria (96h LD50 single dose: 1*107.261cfu/ml; 25 μl) and basal diet feeding for 7 days (prophylactic) or after bacterial inoculation and basal diet feeding for 7 days (therapeutic). Fish fed CE fortified-diet showed significantly (P<0.05) lower mortality, serum cortisol, cytokines, gill and liver reactive oxygen species (ROS) levels, while significantly (P<0.05) higher innate immune parameters than the basal diet-fed fish. CE seemed equally effective as a prophylactic agent to stimulate innate immunity and provide resistance against A. sobria, and a therapeutic agent to reduce A. sobria induced physiological alterations. Chromatography and GC-MS analysis disseminated the presence of 1-tetradecene, 1-heptacosanol, ethane 1,1 diethoxy and cyclotrisiloxane hexamethyl in CE, which were described to manifest antibacterial, antioxidative and immunostimulatory potential.

The present study evaluated the neuroprotective efficacy of Terminalia bellerica and Terminalia catappa fruits through dietary application of different solvent extracts (aqueous, methanol, ethanol, hexane) at various concentrations (0.2, 0.4, 0.8 g kg–1 feed) in an aluminium-induced neurotoxic zebrafish model. Aluminium exposure significantly elevated brain acetylcholinesterase activity, monoamine oxidase activity, and glial fibrillary acidic protein levels in comparison to the control, indicating neurodegeneration. Dietary administration of both plant materials reduced the level of all three biochemical parameters. T. bellerica aqueous extract and T. catappa ethanol extract, both at the concentration of 0.8 g kg–1 feed, showed the best results, restoring acetylcholinesterase, monoamine oxidase, and glial fibrillary acidic protein levels close to those in the control fish. Both T. bellerica and T. catappa fruits may be used as therapeutic agents against neurodegenerative diseases, however, their efficacy depends on the extraction solvent and concentration of dietary supplementation.

The present study investigated the effects of zinc on the hypothalamo-pituitary–gonadal-liver (HPGL) axis of the bagrid catfish Mystus vittatus. Female fish (pre-ovulatory and ovulatory phases) were exposed to zinc sulphate at 1/10th of LC₅₀ (5.62 mg/L) for 60 days and sacrificed at every 15-day interval to collect tissues. Zinc concentration in all tissues was significantly higher in the metal-exposed group at all exposure durations compared to control for both phases. Metallothionein (MT) levels increased in the brain, liver and ovary of fish from both phases with exposure duration. Reactive oxygen species (ROS) generation in the brain, liver and ovary tissues increased with exposure duration at both reproductive phases while serum cortisol levels in ovulatory fish increased significantly compared to pre-ovulatory. Condition factor, gonadosomatic index and hepatosomatic index decreased in Zn-exposed fish. Brain GnRH and kisspeptin levels decreased significantly in the Zn-exposed group for both phases. GnIH was significantly higher in Zn-exposed fish. Serum FSH levels in pre-ovulatory and LH levels in ovulatory fish decreased gradually with an increase in the duration of exposure. Zn exposure reduced vitellogenin (Vtg) and estradiol (E2) in the liver and ovary with an increase in duration from both phases. Ovary maturation-inducing hormone (MIH) levels showed a decrease with exposure duration in ovulatory fish. Moreover, Zn-exposed ovulatory fish showed a degenerated oocyte nucleus due to the disintegration of the nuclear membrane. It might be inferred that Zn altered the HPGL regulatory system of M. vittatus reproduction at both the pre-ovulatory and ovulatory phases.