Apoptosis, a form of programmed cell death, is a critical component in maintaining homeostasis and growth in all tissues and plays a significant role in immunity and cytotoxicity. In contrast to necrosis or traumatic cell death, apoptosis is a well-controlled and vital process characterized mainly by cytoplasmic shrinkage, chromatin condensation, DNA fragmentation, membrane blebbing and apoptotic bodies. Our understanding of apoptosis is partly based on observations in invertebrates but mainly in mammals. Despite the great advantages of fish models in studying vertebrate development and diseases and the tremendous interest observed in recent years, reports on apoptosis in fish are still limited. Although apoptotic machinery is well conserved between aquatic and terrestrial organisms throughout the history of evolution, some differences exist in key components of apoptotic pathways. Core parts of apoptotic machinery in fish are virtually expressed as equivalent to the mammalian models. Some differences are, however, evident, such as the extrinsic and intrinsic pathways of apoptosis including lack of a C-terminal region in the Fas-associated protein with a death domain in fish. Aquatic species inhabit a complex and highly fluctuating environment, making these species good examples to reveal features of apoptosis that may not be easily investigated in mammals. Therefore, in order to gain a wider view on programmed cell death in fish, interactions between the main environmental factors, chemicals and apoptosis are discussed in this review. It is indicated that apoptosis can be induced in fish by exposure to environmental stressors during different stages of the fish life cycle.

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Acrolein is a widely distributed pollutant produced from various sources such as industrial waste, organic combustion, and power plant emissions. It is also intentionally released into irrigation canals to control invasive aquatic plants. Zebrafish (Danio rerio) has a good reputation for being an attractive model organism for developmental and toxicological research. In this study, zebrafish embryos were exposed to acrolein to investigate the cardiotoxic effects. The 96-h LC 50 (median lethal concentration) value of acrolein was determined as 654.385 μg/L. Then, the embryos were treated with the sublethal experimental concentrations of acrolein (1, 4, 16, 64, and 256 μg/L) for 96 h. Embryos were examined at 48, 72, and 96 h post-fertilization (hpf). Acrolein affected the cardiac morphology and function of the embryos. Sinus venosus-bulbus arteriosus (SV-BA) distance of 64 μg/L and 256 μg/L acrolein groups was elongated compared with the control samples. Immunostaining with MF20 antibody clearly exhibited that the atrium positioned posterior to the ventricle which indicated cardiac looping inhibition. Histological preparations also showed the mispositioning and the lumens of the chambers narrowed. Acrolein-induced increased heart rate was noted in the 4, 16, 64, and 256 μg/L treatment groups. Taken together, these results indicated that acrolein disrupted the heart development and cardiac function in zebrafish, suggesting that its water-borne risks should be considered seriously.