It has been known for some time that the process of phagocytosis by mammalian polymorphonuclear leukocytes (PMNs) and macrophages is accompanied by an abrupt increase in oxygen uptake, followed by the production of cytotoxic reactive oxygen intermediates (ROls). The biochemical events associated with this respiratory burst have also been elucidated and will be mentioned in more detail later in this chapter. It is accepted that the first reaction in the respiratory burst is the one electron reduction of oxygen to superoxide (02-)' catalyzed by NADPH oxidase associated with the phagocyte membrane. Superoxide anions are converted to hydrogen peroxide (H20 2) by the cytoplasmic enzyme superoxide dismutase (SOD). Superoxide and, to a great extent, H20 2 are highly reactive and toxic ROIs; H20 2, in conjunction with myeloperoxidase (MPO) and a halide, forms the basis of a potent antibacterial system. I Other toxic ROls can also be generated, such as hydroxyl radicals (.OH) and singlet oxygen (102)' Singly or collectively, these ROls can participate in the cell-mediated destruction of bacteria, fungi, and protozoa. The phagocytes have detoxification enzymes to protect
themselves against autooxidative damage; these include SOD, glutathione peroxidase, catalase, certain vitamins that are radical scavengers, etc. Nevertheless, overproduction of ROls can saturate these protective mechanisms and lead to damage to cells and tissues in the vicinity of the phagocytes. The main purpose of this chapter is to cite evidence for similar respiratory activity in the phagocytes of aquatic invertebrates and fish. The beneficial and the potentially less desirable properties of ROls will be discussed, as will speculation on the physiological consequences of the modulation of ROI production after exposure of aquatic species to environmental chemicals or during the course of certain infectious diseases.