No abstract

No abstract

The aim of this study was to determine whether melatonin (Mel), which is a known antioxidant and free radical scavenger, could perform the role of a preventive agent against the toxic effects of cadmium (Cd2+) on mortality, fish growth, gonadosomatic index (GSI), luteinizing hormone (LH) secretion, the response to hormonal stimulation of spawning, and also tissue accumulation of Cd in Prussian carp females. These females received melatonin implants and were exposed to 0.4 or 4.0 mg/L of Cd (as CdCl2·2.5H2O) over either a 5- or 3-month period, followed by further 2 months of purification in clear water. Negative changes caused by exposure to cadmium in the water were as follows: higher fish mortality, lower body weight, increased accumulation of cadmium in the brain and ovary, lowered GSI, impaired spontaneous LH secretion during exposure, and impaired LH secretion during stimulation of spawning. All of these effects were observed in the group of fish exposed to 0.4 and/or 4.0 mg Cd/L but did not occur or were less pronounced in the groups exposed to cadmium in the presence of melatonin released from the implants. During depuration, in the group of fish which had been exposed to the highest Cd concentration, we observed a significant improvement in fish survival rate, body growth, inhibition of further cadmium accumulation in tissues, and gradual return of spontaneous LH secretion as well as normalization of the GSI value to the control group levels. In conclusion, these findings indicate that melatonin can be a preventive agent for some toxic effects on fish reproduction induced by environmental cadmium contamination.Electronic supplementary materialThe online version of this article (10.1007/s11356-018-1308-8) contains supplementary material, which is available to authorized users.

The oxidative status of the hepatopancreas of Prussian carp females ( Carassius gibelio ) co-exposed to sublethal cadmium in water and melatonin was studied. The activities of antioxidant enzymes such as glutathione reductase (GR), glutathione peroxidase (GPx), and superoxide dismutase (SOD) as well as the concentration of reduced glutathione (GSH) were measured in homogenates of the hepatopancreas. Furthermore, concentrations of cadmium (Cd), zinc (Zn), copper (Cu), and iron (Fe) in the hepatopancreas were assayed. These females received melatonin implants and were exposed to 0.4 mg/L or 4.0 mg/L Cd in water for either a 13- or a 7-week period, followed by further 6 weeks of purification in clear water. Exposure to Cd influenced the increase in this metal concentration in fish hepatopancreas. In contrast, the fish exposed to cadmium with additional administration of melatonin had a lower accumulation of this metal. Exposure to Cd caused the increase in GSH content and the activity of GR, and a reduction in GPx activity, whereas the SOD activity varies depending on the exposure time on cadmium. In the hepatopancreas of fish treated with Cd alone, the content of Cu and Zn were increased and that of Fe was changed. After melatonin administration to Cd-exposed fish, a decrease in copper and zinc hepatopancreas content was noted. The present findings imply that melatonin co-treatment can effectively protect the fish against the toxic effects of cadmium on endogenous antioxidant status in hepatopancreas tissues and variations in metal concentration, such as Zn, Cu, and Fe.

No abstract

ABSTRACT:The effects of serotonin (5-HT), GnRH analogue (D-Ala 6 LHRH, GnRH-A) and dopamine antagonist -pimozide (PIM), on luteinizing hormone (LH) release in mature Prussian carp female (Carassius gibelio Bloch) were examined at the time of gonad recrudescence. Fish were intraperitoneally injected with 5-HT (10 mg/kg), GnRH-A (20 μg/kg) or PIM (5 mg/kg) or the combinations: 5-HT+GnRH-A, 5-HT+PIM, 5-HT+GnRH-A+PIM. Before the injection and 3, 6, 12 or 24 h after treatment blood samples were collected for LH levels determination by ELISA method. The analysis of LH concentrations, expressed as the percentage of pre-treatment, showed that serotonin alone had no influence on the spontaneous LH release, however the additive effects of serotonin and GnRH-A was observed. Serotonin potentiated the GnRH-A-stimulated LH release and potentiated also the effect of PIM. Extremely strong response to PIM and also to the combination with GnRH-A masked the participation of serotonin in the process of LH release in fish with recrudescing gonads. The interaction of serotonin GnRH-A and PIM in the control of LH release is discussed.

No abstract

No abstract