Death and senescence - Adults Fishes

Death and senescence

Death in fishes usually results from predation, accident, opportunistic pathogens, or accumulated somatic mutations that lead to a slow decline in health and an increased susceptibility to environmental factors. However, some fishes age via the “programmed death” process of senescence that is more typical of mammals such as ourselves. Senescence refers to age-related changes that have an adverse effect on an organism and that increase the likelihood of its death (Finch 1990). Senescence includes the metabolic and anatomical breakdown that occurs in older adult animals following maturation and reproduction. Pacific salmon provide a dramatic example. Reproductively migrating fish in peak physical condition enter their natal river, mature, spawn, break down anatomically and physiologically, and die in a matter of weeks. Many of the anatomical and physiological changes that occur can be linked to the combined effects of overproduction of steroids and starvation. Interrenal cells, which are steroid-producing cells associated with the kidney and are homologous with the adrenal cortex of mammals, secrete corticosteroids, producing blood levels of these substances five or more times higher than normal levels. This hyperadrenocorticism results in rapid degenerative changes in the heart, liver, kidney, spleen, thymus, and coronary arteries; the latter degeneration is strikingly similar to coronary artery disease in humans. The digestive tract including intestinal villi degenerates, fat reserves are depleted, and feeding ceases. Fungal infections and reduced resistance to bacteria occur, indicating loss of immune function. A conflict between reproduction and survival is evident in the breakdown of the immune system: elevated corticosteroids apparently serve to speed the mobilization of stored energy into reproductive activity, but have the “side effect” of suppressing immune function. In naturally spawning Pacific salmons,

these side effects are irreversible. Castrated males and females do not produce the elevated corticosteroids, and do not spawn, but instead continue to grow to twice the length and live twice as long as intact fish. Precocious males, those that matured as parr and bypassed the smolt and marine phases, may survive spawning and breed again the next year (Finch 1990).

Equally spectacular senescence occurs in several other fish taxa. Reproduction in both parasitic and nonparasitic lampreys involves maturation accompanied by cessation of feeding and atrophy of most internal organs with the exception of the heart and gonads. Fats and muscle proteins are metabolized or transformed into gonadal products. Both males and females die shortly after spawning, probably from starvation. Anguillid eels live as juveniles for many years in rivers and lakes. They then undergo a reproductive metamorphosis that includes enlargement of eyes, changes in body coloration and fin proportions, gut degeneration, and cessation of feeding. After a reproductive migration to the sea that may take them thousands of kilometers, all adults presumably die (see  Catadromy). Laboratory manipulation of hormone functions indicate that, as with salmons, rapid senescence results from elevated corticosteroids and starvation. During maturation, conger and snipe eels also experience gut atrophy and in addition lose their teeth. The Ice Goby, Leucosparion petersi, which enters fresh water to spawn and then dies, develops enlarged adrenals and splenic degeneration. More gradual senescence has been observed in many multiply spawning species, such as herrings, haddocks, Guppies and other livebearers,

annual killifishes, and Medaka. Anatomical and physiological indicators of gradual senescence include reduced or even negative length and weight change, reduced egg output, corneal clouding, disordered scales, malignant growths such as melanomas, spinal deformities, and impaired regenerative capability. Such senescent changes are more common in small, short-lived species that mature at relatively early ages (Lindsey 1988; Finch 1990; Kamler 1991).