Abstract
BackgroundIncreasing evidence demonstrate that cadmium (Cd) has adverse effects on the mammalian reproductive system. However, the mechanisms underlying the effects of Cd on ovarian function and the strategies to reverse these effects have not been fully elucidated.MethodsIn this study, 60 CD-1 mice were divided into four groups (control, melatonin, Cd, Cd with melatonin). During the treatment for 14 days, body weight was measured every 2 days. After the treatment, ovaries were isolated and weighted to observe the morphological and biological characteristics. Statistical analyses were performed using one-way ANOVA followed by Fisher’s-multiple range test or chi-squared test, A P value < 0.05 indicated statistical significance.ResultsWe observed that Cd exposure induced ovulatory dysfunction, demonstrated by the reduced number of ovulated oocytes numbers in the Cd group. However, this endoplasmic reticulum (ER) pathway was activated in the Cd-exposed ovaries and the expression of GRP78, ATF4, CHOP, and p-JNK was upregulated, which was reversed by treatment with melatonin. Furthermore, we found that melatonin inhibited Cd-induced activation of cleaved caspase-3, restored the ratio of Bax/Bcl-2, and ultimately decreased the apoptosis of granular cells as detected by TUNEL staining.ConclusionCollectively, our findings reveal that melatonin attenuated Cd-induced ovulation dysfunction and cell apoptosis by inhibiting the activation of the ER pathway. Thus, melatonin can be a potential agent to protect mammalian ovaries against Cd toxicity.
Highlights
Cadmium (Cd) is a ubiquitous environmental contaminant, which cannot be degraded [1]
We found that Cd activated the endoplasmic reticulum (ER) pathway, which resulted in cell apoptosis in the ovary
Melatonin reverses the ovulatory dysfunction in cdtreated mice The body weights of the mice were recorded every other day
Summary
Cadmium (Cd) is a ubiquitous environmental contaminant, which cannot be degraded [1]. Exposure to Cd in the general population occurs through the consumption of polluted food or water, cigarette smoking and the inhalation of contaminated air [2]. Mammalian ovaries contain oocytes at different stages of development, and somatic cells of various types. Increasing evidence demonstrates the reproductive toxicity of Cd in female animals and humans. Exposure to Cd damaged the structure of the ovary, and caused irregular estrous cycles and abnormal hormone synthesis and follicle development [7, 8]. A recent study reported the toxicity of Cd on the reproductive system of female birds demonstrated by the ultra-structural changes in the ovarian cells [9]. Increasing evidence demonstrate that cadmium (Cd) has adverse effects on the mammalian reproductive system. The mechanisms underlying the effects of Cd on ovarian function and the strategies to reverse these effects have not been fully elucidated
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