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Cortisol is responsible for positive and negative effects in the ovarian maturation induced by the exposure to acute stressors in Nile tilapia, Oreochromis niloticus
- Gennotte, Vincent, Sawadogo, Philippe, Milla, Sylvain, Kestemont, Patrick, Mélard, Charles, Rougeot, Carole
- Fish physiology and biochemistry 2012 v.38 no.6 pp. 1619-1626
- Oreochromis niloticus, acute effects, acute exposure, aquariums, body weight, cortisol, fecundity, females, fiberglass, fish, hatching, oocytes, ovulation, sodium chloride, tanks, vehicles
- The aim of the present study was to evaluate the effect of acute stress and cortisol injection on oocyte final maturation process in female Nile tilapia (Oreochromis niloticus). Handling followed by a prophylactic treatment (0.3 mL L⁻¹ H₂O₂, 5 g L⁻¹ NaCl solution during 30 min) and an environmental change (transfer from a 2 m³ fibreglass square tank to 50 L aquaria) were used as acute stressors and compared to a single cortisol injection (0.5 or 5 mg kg⁻¹ body weight). For both acute stress and cortisol injection (0.5 mg kg⁻¹ body weight), serum cortisol level was significantly increased from 2.3 to 134.1 ng mL⁻¹ 1 h post-stress/injection and returned to a resting basal value 24 h after the stress/injection. In fish injected with 5 mg kg⁻¹ body weight cortisol, mean serum cortisol level reached a peak up to 2500 ng mL⁻¹ 1 h after injection. 63 % of the females (mean body weight: 242 ± 4 g) submitted to the acute stress ovulated within 72 h after the stress. In the same way, cortisol injection (5 mg kg⁻¹ body weight) at the 10th day of the maturation cycle led to a twofold reduction of the time before ovulation compared to vehicle injected control fish. Relative and total fecundity were significantly decreased in females submitted to an acute stress or cortisol injected at 5 mg kg⁻¹ body weight, but not fertilization or hatching rates. In conclusion, acute stress and cortisol induction exert both positive and negative effects on the final reproductive process in O. niloticus, and cortisol is the endocrine mediator causing these changes.