Although several studies have been conducted to study leptin function, information is very scarce on the molecular mechanism of leptin in fatty acid β-oxidation and oocytes maturation in fish. In this study, we investigated the potential role of fatty acid β-oxidation in leptin-mediated oocytes maturation in Pelteobagrus fulvidraco. Exp. 1 investigated the transcriptomic profiles of ovary and the differential expression of genes involved in β-oxidation and oocytes maturation following rt-hLEP injection; rt-hLEP injection was associated with significant changes in the expression of genes, including twenty-five up-regulated genes (CPT1, Acsl, Acadl, Acadm, Hadhb, Echsl, Hsd17b4, Acca, PPARα, CYP8B1, ACOX1, ACBP, MAPK, RINGO, Cdc2, MEK1, IGF-1R, APC/C, Cdk2, GnRHR, STAG3, SMC1, FSHβ and C-Myc) and ten down-regulated gene (PPARγ, FATCD36, UBC, PDK1, Acads, Raf, Fizzy, C3H-4, Raf and PKC), involved in fatty acid β-oxidation and oocytes maturation. In Exp. 2, rt-hLEP and specific inhibitors AG490 (JAK-STAT inhibitor) were used to explore whether leptin induced oocytes maturation, and found that leptin incubation increased the diameters of oocytes and percentage of germinal vesicle breakdown (GVBD)-MII oocytes, up-regulated mRNA levels of genes involved in oocytes maturation and that leptin-induced oocyte maturation was related to activation of JAK-STAT pathway. In Exp. 3, primary oocytes of P. fulvidraco were treated with (R)-(+)-etomoxir (an inhibitor of β-oxidation) or l-carnitine (an enhancer of β-oxidation) for 48 h under rt-hLEP incubation. Exp. 3 indicated that the inhibition of fatty acid β-oxidation resulted in the down-regulation of gene expression involved in oocytes maturation, and repressed the leptin-induced up-regulation of these gene expression. Activation of fatty acid β-oxidation improved the maturation rate and mean diameter of oocytes, and up-regulated gene expression involved in oocytes maturation. Leptin is one of the main factors that links fatty acid β-oxidation with oocyte maturation; β-oxidation is essential for leptin-mediated oocyte maturation in fish.

Cadmium (Cd) is an environmental contaminant that presents significant threat to aquatic organisms. This study was conducted to examine histological structure as well as antioxidative and inflammatory responses in spleen and head kidney of yellow catfish after 8 weeks of exposure to 50 and 200 µg/L Cd2+. It showed that Cd2+ exposure induced Cd accumulation and impaired histological structure in the spleen and head kidney. For antioxidative response: in the spleen, sod1 expression was significantly upregulated by 50 and 200 µg/L Cd2+, while cat, gpx1, gstω1 and nrf2 expressions were up-regulated by 50 µg/L Cd2+ but not by 200 μg/L Cd2+; in the head kidney, these genes were down-regulated by Cd2+ exposure. For inflammatory response: in the spleen, the expression of il-8, tnf-α and il-10 were up-regulated by 50 µg/L Cd2+ but not by 200 μg/L Cd2+, while the expression of tor and tgf-β were significantly up-regulated only by 200 µg/L Cd2+; in the head kidney, Cd2+ exposure down-regulated the expression of il- 1β, il-8, tor, tnf-α, il-10 and tgf-β. Therefore, this study suggested that Cd2+ exposure could cause Cd accumulation in the spleen and head kidney, and induced histological lesions, antioxidative and inflammatory responses in both tissues.