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Vast stretches of open water bodies are gradually becoming hypoxic as a result of depletion of oxygen levels mainly due to various human anthropogenic activities. This problem of hypoxic stress on the fish population is likely to be exacerbated soon since the aquatic hypoxic environment is continuously spreading over vast areas worldwide. In recent years, various harmful effects of hypoxia to bony fishes have been reported, such as the restriction of energy-consuming metabolic processes, arrest of the growth of ovary and testes that are associated with endocrine disruption, loss of sperm and egg quality, inhibition of fertilization, hatching success, and also the reduction of larval survivability, thereby impairment of overall reproductive and developmental processes in fish. Disruption of the brain-pituitary-gonad axis, and certain enzymes related to steroidogenesis and vitellogenesis in fish have also been reported as the primary targets for an endocrine malfunction during hypoxia. Hypoxia-sensitive downregulation of key genes responsible for controlling sex hormones' synthesis has been documented in certain bony fishes. Further, continuous exposure to hypoxia was reported to induce early expression of pro-apoptotic/tumor suppressor p53 genes, thereby causing immense cell death in hypoxic embryos. However, the cellular responses to long-term hypoxia exposure and the degree of reproductive impairments in bony fishes are still not adequate to figure out the actual underlying mechanisms. The present review intends to highlight the current knowledge about the detrimental impact of chronic/acute hypoxia at different stages of fish reproduction and the associated underlying molecular mechanisms.

Vast stretches of open water bodies are gradually becoming hypoxic as a result of depletion of oxygen levels mainly due to various human anthropogenic activities. This problem of hypoxic stress on the fish population is likely to be exacerbated soon since the aquatic hypoxic environment is continuously spreading over vast areas worldwide. In recent years, various harmful effects of hypoxia to bony fishes have been reported, such as the restriction of energy-consuming metabolic processes, arrest of the growth of ovary and testes that are associated with endocrine disruption, loss of sperm and egg quality, inhibition of fertilization, hatching success, and also the reduction of larval survivability, thereby impairment of overall reproductive and developmental processes in fish. Disruption of the brain-pituitary-gonad axis, and certain enzymes related to steroidogenesis and vitellogenesis in fish have also been reported as the primary targets for an endocrine malfunction during hypoxia. Hypoxia-sensitive downregulation of key genes responsible for controlling sex hormones' synthesis has been documented in certain bony fishes. Further, continuous exposure to hypoxia was reported to induce early expression of pro-apoptotic/tumor suppressor p53 genes, thereby causing immense cell death in hypoxic embryos. However, the cellular responses to long-term hypoxia exposure and the degree of reproductive impairments in bony fishes are still not adequate to figure out the actual underlying mechanisms. The present review intends to highlight the current knowledge about the detrimental impact of chronic/acute hypoxia at different stages of fish reproduction and the associated underlying molecular mechanisms. [ABSTRACT FROM AUTHOR]

• Chronic noise exposure dysregulates the neuroendocrine system leading to hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis. • Stress hormones adversely affect cell biology and neuronal circuitry leading to impairment in behavior. • Enduring dysregulation of the HPA-axis is the most mechanism associated with the harmful noise effects. • Noise stress shows a causative association with diverse landmarks of Alzheimer's disease (AD) with a hyper-susceptibility in females. • Functional and Neuroimaging studies are suggested to quantify the contribution of noise in predisposing AD in human. This review examines the adverse impacts of different noise exposure paradigms on the neuroendocrine system, hippocampal and neocortical structures, cognitive performances, and the development of Alzheimer's disease (AD)-like neuropathological changes in the brain of laboratory animals. Studies were reviewed in three periods during the lifespan including: adult animals exposed to noise, female rodents exposed to noise during gestation, and offspring exposed to noise during the prenatal period. Findings imply that chronic noise exposure dysregulates the neuroendocrine system leading to hyperactivation of the sympathetic divisions of the autonomic nervous system (i.e., the hypothalamic-pituitary-adrenal (HPA)-axis), and increases stress hormones that affect brain and behaviour. Enduring dysregulation of the HPA-axis was the most discussed mechanism for the harmful effect of noise during the lifespan. Studies also suggest a causative association of noise with diverse indicators of the AD-like neuropathology in rodents and a hypersusceptibility in females. The results indicate the importance of future neuroimaging studies to quantify the potential contribution of noise in predisposing cognitive decline and preclinical signs of dementia in humans. [ABSTRACT FROM AUTHOR]

The hypothalamic–pituitary–adrenal (HPA) axis, which plays a major role in the response to stress, and the hypothalamic–pituitary–gonadal (HPG) axis are closely linked with the ability to inhibit the other. Testosterone, a product of the HPG, has many beneficial effects beyond its functions as a sex hormone including anti-anxiety properties. In this study we examined the effect of stress exposure on gonadal hormones, and their efficacy in modulating anxiety-like response in an animal model of PTSD. Male rats were exposed to predator scent stress, followed by analysis of brain expression of androgen receptor (AR) receptor and estrogen receptor α (ERα). The behavioral effects of immediate treatment with testosterone, testosterone receptor antagonist (flutamide) or vehicle were evaluated using the elevated plus-maze, acoustic startle response and trauma-cue response. Levels of circulating corticosterone and testosterone were also measured after treatment. The behavioral effects of delayed testosterone treatment were explored in the same manner. We report that animals whose behavior was extremely disrupted (EBR) selectively displayed significant down-regulation of AR and ERα in the hippocampus. Immediate treatment with flutamide or delayed treatment with testosterone significantly increased prevalence rates of minimal behavioral response (MBR) and decreased prevalence of EBR with favorable behavioral results. Testosterone levels were higher in control un-exposed animals, while corticosterone was higher in control exposed animals. This study suggests that gonadal steroid hormones are involved in the neurobiological response to predator scent stress and thus warrant further study as a potential therapeutic avenue for the treatment of anxiety-related disorders. [ABSTRACT FROM AUTHOR]

• Early life Hg exposure impairs reproduction in adult zebrafish. • Early life Hg exposure has intergenerational effect on reproduction of F 1 females. • Reproductive damage caused by early life Hg exposure is recovered in F 1 males. • Reproductive damage caused by early life Hg exposure is recovered in F 2 females. Mercury (Hg) is a global pollutant that poses potential threats to health of fishes. Although effects of Hg on reproduction of fishes have been documented, little is known about effects of exposure to Hg2+ during early life stages on subsequent reproductive fitness of adults or whether these effects can be transferred to offspring. In this study, zebrafish embryos were exposed to environmentally relevant concentrations of Hg2+ (0.6, 3 or 15 μg/L) for 5 days and then depurated in clean water for another 115 days. Exposure to Hg2+ during early life stages disturbed the balance of sex hormones and gametogenesis by altering expression of mRNA for genes involved in the hypothalamic-pituitary-gonadal axis, which resulted in delayed gonadal development and lesser gonado-somatic index, thereby resulting in lesser fecundity. A similar, but less pronounced effect was observed in F 1 females that were not exposed directly to Hg, whereas such damage was neither observed in F 1 males nor either sex during the F 2 generation. Exposure to Hg2+ during early life can impair subsequent reproduction in adults and has intergenerational effects on F 1 females, but this reproductive damage can be recovered in F 1 males and in F 2 females. [ABSTRACT FROM AUTHOR]