Environmentally relevant concentrations of Mn2+ disrupts the endocrine regulation of growth in juvenile Yunlong groupers (Epinephelus moara♀×Epinephelus lanceolatus♂).

Even though manganese is a bioelement essential for metabolism, excessive manganese levels in water can be detrimental to fish development and growth. Therefore, the aim of this study was to evaluate the effects of Mn2+ (0, 0.5,1, 2, and 4 mg·L-1) exposure for 30 d on the growth performance, growth hormone/insulin-like growth factor (GH/IGF) axis, hypothalamic-pituitary-thyroid (HPT) axis, and monoaminergic neurotransmitters of Epinephelus moara♀×Epinephelus lanceolatus♂(Yunlong grouper). Compared with the control and low Mn2+concentration groups of (0.5 and 1 mg·L-1), the high concentration of Mn2+ (4 mg·L-1) significantly reduced body weight (BW), body length (BL), weight gain rate (WGR), and specific growth rate (SGR), increased the feed coefficient rate (FCR) and mortality of Yunlong groupers (P < 0.05). Further, the levels of GH and IGF, along with the expression of ghra and ghrb were significantly reduced after exposure to 2 and 4 mg·L-1 Mn2+for 30 d, whereas the expression of sst5 was significantly up-regulated after exposure to 2 and 4 mg·L-1 Mn2+for 20 and 30 days. Moreover, Mn2+exposure increased thyroid hormone (T3) and thyroid stimulating hormone (TSH) contents, accompanied by increased mRNA levels of dio1 and dio2, however, the T4 level was decreased. Finally, dopamine (DA) and serotonin (5-HT) levels significantly decreased after long-term exposure to higher concentrations of Mn2+, and the levels their metabolites changed as well, suggesting that the synthesis and metabolism of DA and 5-HT were affected. Accordingly, changes in the GH/IGF and HPT axes-related parameters may be the cause of growth inhibition in juvenile groupers under Mn2+ exposure, indicating that the relationship between endocrine disorder and growth inhibition should not be ignored.

Bioaccumulation of manganese and its effects on oxidative stress and immune response in juvenile groupers (Epinephelus moara ♀ × E. lanceolatus ♂).

We evaluated the effects of Mn in juvenile Yunlong groupers (Epinephelus moara ♀ × E. lanceolatus ♂). The groupers were exposed to Mn2+ (0, 0.5, 1, 2, and 4 mg/L) for 30 days after which they were assessed. The results indicate the accumulation of Mn in fish depended on dose and time. Mn2+ accumulation in tissues occurred in the following order: liver > gills > intestine > muscle. The concentrations of SOD and CAT in the fish significantly increased after 10 and 20 days of treatment with 4 mg/L Mn2+ but decreased after 30 days. Similarly, GSH and GPx levels increased after 10 days of exposure to 2 and 4 mg/L Mn2+ but decreased after 20 and 30 days of exposure. Additionally, malondialdehyde levels significantly increased after exposing the fish to 2 and 4 mg/L Mn2+ for 10, 20, and 30 days. In addition, liver HSP70 and HSP90 levels significantly increased at days 20 and 30 in all fish exposed to Mn2+. In addition, when Mn2+ concentration was 1, 2, and 4 mg/L, liver C3 and C4 levels were significantly increased after 10, 20, and 30 days. Conversely, the levels of LZM and IgM significantly decreased. Mn2+ also significantly upregulated the expression of genes associated with immunity (tlr3, tnf-α, il-1ß, and il-6) in the fish, which suggests that it induces immunotoxicity by altering the immune response. Overall, the findings showed that Mn2+ can disrupt grouper health by bioaccumulating in the fish and subsequently inducing oxidative stress and immune responses. These results can help elucidate the mechanism by which manganese induces toxicity in marine fish. Additionally, they provide a new perspective regarding the detrimental effects of heavy metals in fish.

Alterations in hematological and biochemical parameters, oxidative stress, and immune response in Takifugu rubripes under acute ammonia exposure.

Ammonia is a major pollutant in aquatic environments and poses a considerable threat to the survival of fish. In this study, we investigated the toxic effects of ammonia on the hematological and biochemical parameters, oxidative stress, and immune responses in Takifugu rubripes. Juvenile T. rubripes (average weight 246.17 ± 3.54 g) were exposed to different concentrations of ammonia (0, 5, 50, 100, and 150 mg/L) for 96 h. The results showed that the hematological parameters (hemoglobin, hematocrit, red blood cell, and white blood cell count) were significantly reduced in response to ammonia exposure. Of the plasma components, such as serum total protein, albumin, glucose, glutamic-oxalacetic transaminase, and glutamic-pyruvic transaminase, were significantly altered in response to ammonia exposure. Additionally, the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx) were increased after exposure to low concentration ammonia exposure. However, when fish were exposed to a high concentration of ammonia, these parameters showed the opposite trend, suggesting that an increase in antioxidant enzymes during the early stages of ammonia exposure may contribute to the removal of the induced reactive oxygen species (ROS) and protect the cells from oxidative damage. However, as the ammonia concentration and exposure time increased, the overproduction of ROS accelerated the depletion of antioxidant enzymes. Ammonia exposure significantly increased the expression of heat shock proteins (HSP70 and HSP90). Ammonia poisoning elevated gene expressions of TLR-3, TNF-α, IL-6, IL-12, and IL-1ß in the gills, causing an inflammatory response. Our findings provide new insights into the mechanisms involved in ammonia-induced aquatic toxicology in marine fish, which may aid in their captive management.