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.
Highlights
Cadmium (Cd2+) is one of the most important toxic heavy metals and a non-essential element widely used in industrial and agricultural practices such as fertilizers and pesticides (Satarug et al 2003)
Successive measurements of fish body weight showed gradual inhibition of their growth in the group exposed to the highest cadmium dose in water (4.0 mg Cd/L)
At the end of the experiment, the average body weight of fish in the group exposed to 4.0 mg Cd/L was significantly lower in comparison to the 0.4 mg Cd/L, Mel, and blank groups (Table 1)
Summary
Cadmium (Cd2+) is one of the most important toxic heavy metals and a non-essential element widely used in industrial and agricultural practices such as fertilizers and pesticides (Satarug et al 2003). Numerous studies carried out on fish proved the toxic effect of cadmium on the nervous, endocrinal, and reproductive systems. The hypothalamo-pituitarygonadal axis seems to be the main target of toxic cadmium influence. This metal may act at various sites on this axis altering the reproductive endocrine function (Tilton et al 2003). It has been shown that cadmium in fish affects LH secretion, causing hypertrophy, vacuolization, and degeneration of gonadotropic cells (Szczerbik et al 2006). Numerous experiments have proved that cadmium has negative effects on ovarian functions in fish. This metal causes the ovary structure to disintegrate, oolemma necrosis, and follicular cells hypertrophy. In the early gonadal recrudescence phase, cadmium increased steroid ovarian hormone secretion and the premature growth of the ovary (El-Ebiary et al 2013)
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