Hypoxia inhibits fish spawning via LH-dependent final oocyte maturation.

To evaluate the effects of long term hypoxia exposure on fish spawning, mature common carp, Cyprinus carpio carpio (Linnaeus) were subjected to either normoxia (7.4+/-0.2 mgO(2)mg O(2) L(-1)) or hypoxia (1.0+/-0.2 mgO(2)O(2) L(-1)) for more than two months. Gonadosomatic index (GSI), and concentrations of serum luteinizing hormone (LH), testosterone (T), and estroldiol (E2) were measured and gonad histology examined. Hypoxia inhibits fish spawning even though the gonad and oocytes developed under hypoxia exposure. LH levels of female carp were significantly decreased upon chronic exposure to hypoxia, and the final oocyte maturation in hypoxic females was significantly retarded. The results indicated that hypoxia may inhibit fish spawning through LH-dependent final oocyte maturation. In addition, no courtship was observed in hypoxic males. In conclusion, hypoxia impairs fish ovulation and, therefore, spawning and reproduction. LH levels were reduced leading to a failure of oocyte maturation. This, along with a lack of courtship by males may be the major mechanisms involved in hypoxic inhibition of reproduction in carp.

Ammonia excretion in rainbow trout (Oncorhynchus mykiss): evidence for Rh glycoprotein and H+-ATPase involvement.

Branchial ammonia transport in freshwater teleosts is not well understood. Most studies conclude that NH(3) diffuses out of the gill and becomes protonated to NH(4)(+) in an acidified gill boundary layer. Rhesus (Rh) proteins are new members of the ammonia transporter superfamily and rainbow trout possess genes encoding for Rh30-like1 and Rhcg2. We identified seven additional full-length trout Rh cDNA sequences: one Rhag and two each of Rhbg, Rhcg1, and Rh30-like. The mRNA expression of Rhbg, Rhcg1, and Rhcg2 was examined in trout tissues (blood, brain, eye, gill, heart, intestine, kidney, liver, muscle, skin, spleen) exposed to high external ammonia (HEA; 1.5 mmol/l NH(4)HCO(3), pH 7.95, 15 degrees C). Rhbg was expressed in all tissues, Rhcg1 was expressed in brain, gill, liver, and skin, and Rhcg2 was expressed in gill and skin. Brain Rhbg and Rhcg1 were downregulated, blood Rh30-like and Rhag were downregulated, and skin Rhbg and Rhcg2 were upregulated with HEA. After an initial uptake of ammonia into the fish during HEA, excretion was reestablished, coinciding with upregulations of gill Rh mRNA in the pavement cell fraction: Rhcg2 at 12 and 48 h, and Rhbg at 48 h. NHE2 expression remained unchanged, but upregulated H(+)-ATPase (V-type, B-subunit) and downregulated carbonic anhydrase (CA2) expression and activity were noted in the gill and again expression changes occurred in pavement cells, and not in mitochondria-rich cells. Together, these results indicate Rh glycoprotein involvement in ammonia transport and excretion in the rainbow trout while underscoring the significance of gill boundary layer acidification by H(+)-ATPase.