Abstract

Chloramine-T, a treatment chemical used in salmonid hatcheries, can cause significant growth deceleration as a result of inefficiency in feed conversion. A reasonable hypothesis proposes that the physiological mechanism involves the stress response, and two trials were designed to asses this. In the first trial, tanks of healthy juvenile rainbow trout Oncorhynchus mykiss were exposed to chloramine-T (10 mg/L) or formalin (200 mg/L) for 1 h once per week for four weeks. The effect of this treatment on the primary stress response was evaluated by measuring circulating cortisol levels with a radioimmunoassay technique. Blood cortisol levels were analyzed at 1, 24, and 96 h after each treatment and compared with preexposure baseline values and with values obtained from sham-treated fish. At 1 h, fish in all treatment categories had elevated cortisol levels compared with baseline values, but values in those fish treated with chemicals were no different from those that were sham treated. Cortisol levels returned to near baseline by 24 h after treatment. In the second experiment, the effect of twice weekly 1-h exposure to chloramine-T (10 mg/L) on secondary stress indices of rainbow trout was probed during an 11-week growth trial by measuring hematocrit, plasma glucose, sodium, and chloride levels in treated, untreated, and sham-treated fish. No evidence of a secondary stress response could be detected in fish treated with chloramine-T when they were compared with either control group. We conclude that intermittent exposure to chloramine-T at 10 mg/L does not elicit a primary or secondary stress response in rainbow trout and that stress is not the mechanism responsible for growth deceleration in treated fish.

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