Plasma biochemical changes, ovarian steroidogenesis, and ultrastructural and histological observations during preovulatory ovarian atresia in captive white sturgeon (Acipenser transmontanus Richardson)

Preovulatory ovarian atresia in white sturgeon has been observed under culture conditions, and it has been associated with unseasonably high or constant temperatures during oocyte polarization phase. Our objectives were to examine histological and ultrastructural changes in the ovarian follicles of females exposed to elevated temperature at different stages of oogenesis, concomitant changes in plasma sex steroids and vitellogenin levels, and in vitro follicular steroidogenesis. Gravid white sturgeon females were exposed to warm water (≥18°C) either before or after acquisition of oocyte maturational competence while control females were held at seasonal temperature (rising from 10°C in December to 16°C in May). Ovarian follicles (morphometry, in vitro steroid production, electron microscopy and histology) and blood (plasma estradiol, E2, androgens, A, vitellogenin, VTG) were sampled with 2--4 weeks intervals. Females kept at seasonal water temperature completed oocyte development, and normal ovulatory response to hormonal treatment and production of viable larvae were demonstrated. Fish exposed to warm water prior to acquisition of maturational competence exhibited arrested germinal vesicle migration, GVM, followed by ovarian atresia. Plasma E2 and VTG declined at a significantly faster rate than control. Atresia was associated with low plasma E2; A and VTG levels. Fish exposed to warm water after acquisition of maturational competence exhibited accelerated GVM and reached pre-spawning stage. Plasma E2 and VTG in these fish decreased at a significantly faster rate than in females kept at seasonal temperature, and no ovulatory response was obtained after GnRHa injection. The temperature-sensitive stage in late oogenesis of white sturgeon appears to occur during a period of protein synthesis required for the oocytes to reach maturational competence. Morphologically, the onset of follicular atresia is manifested by hypertrophy of granulosa layer, followed by digestion of the vitelline envelope, disruption of cytoplasmic cortex, and nuclear membrane dissolution. This is followed by rapid disintegration of the yolk platelets and formation of corpora atretica. Ultrastructurally, the first sign of atresia is hypertrophy of transformed granulosa cells is associated with accumulation of cytoplasmic vacuoles filled with granular material. The transformed granulosa cells secrete the granular material and, as a result, the chorion is liquefied. Concomitantly, the oocyte undergoes GVBD, the cytoplasm cortex is distorted, and the oolema disintegrates. Phagocytosis of oocyte content is carried out by transformed granulosa although the lymphocytes also infiltrate the thecal layer and may take part in oocyte resorption.