The immunotoxic effects of some anthropogenic pollutants on aquatic organisms are among the causes of concern over the presence of these pollutants in the marine environment. The immune system is part of an organism’s biological defense necessarily for homeostasis. Thus, the immunotoxicological impacts on aquatic organisms are important to understand the effects of pollutant chemicals in the aquatic ecosystem. When aquatic organisms are exposed to pollutant chemicals with immunotoxicity, it results in poor health. In addition, aquatic organisms are exposed to pathogenic bacteria, viruses, parasites, and fungi. Exposure to pollutant chemicals has reportedly caused aquatic organisms to show various immunotoxic symptoms such as histological changes of lymphoid tissue, changes of immune functionality and the distribution of immune cells, and changes in the resistance of organisms to infection by pathogens. Alterations of immune systems by contaminants can therefore lead to the deaths of individual organisms, increase the general risk of infections by pathogens, and probably decrease the populations of some species. This review introduced the immunotoxicological impact of pollutant chemicals in aquatic organisms, including invertebrates, fish, amphibians, and marine mammals; described typical biomarkers used in aquatic immunotoxicological studies; and then, discussed the current issues on ecological risk assessment and how to address ecological risk assessment through immunotoxicology. Moreover, the usefulness of the population growth rate to estimate the immunotoxicological impact of pollution chemicals was proposed.

Although pregnant women's fish consumption is beneficial for the brain development of the fetus due to the DHA in fish, seafood also contains methylmercury (MeHg), which adversely affects fetal brain development. Epidemiological studies suggest that high DHA levels in pregnant women's sera may protect the fetal brain from MeHg-induced neurotoxicity, but the underlying mechanism is unknown. Our earlier study revealed that DHA and its metabolite 19,20-dihydroxydocosapentaenoic acid (19,20-DHDP) produced by cytochrome P450s (P450s) and soluble epoxide hydrolase (sEH) can suppress MeHg-induced cytotoxicity in mouse primary neuronal cells. In the present study, DHA supplementation to pregnant mice suppressed MeHg-induced impairments of pups' body weight, grip strength, motor function, and short-term memory. DHA supplementation also suppressed MeHg-induced oxidative stress and the decrease in the number of subplate neurons in the cerebral cortex of the pups. DHA supplementation to dams significantly increased the DHA metabolites 19,20-epoxydocosapentaenoic acid (19,20-EDP) and 19,20-DHDP as well as DHA itself in the fetal and infant brains, although the expression levels of P450s and sEH were low in the fetal brain and liver. DHA metabolites were detected in the mouse breast milk and in human umbilical cord blood, indicating the active transfer of DHA metabolites from dams to pups. These results demonstrate that DHA supplementation increased DHA and its metabolites in the mouse pup brain and alleviated the effects of MeHg on fetal brain development. Pregnant women's intake of fish containing high levels of DHA (or DHA supplementation) may help prevent MeHg-induced neurotoxicity in the fetus.