Abstract
Zearalenone (ZEA) mainly injures the reproductive system of mammals. In the present study, we aimed to explore the mechanism by which zinc inhibits ZEA-induced reproductive damage in KK-1 cells for the first time. The results shown that both zinc sulfate and zinc gluconate addition increased the intracellular zinc concentration and influenced the expression of zinc transporters (Slc30a1 and Slc39a1) in a time-dependent manner. Co-incubation of zinc with ZEA significantly reduced the ZEA-induced reactive oxygen species and malondialdehyde elevation by promoting the transcription of Mtf1 and Mt2. Meanwhile, two different zincs inhibited the ZEA-induced loss of mitochondrial membrane potential and elevation of late-stage apoptosis via activating the mitochondrial apoptotic pathway by recovering the mRNA and protein expression of pro-apoptotic genes (Bax, Casp3, Casp9). Zinc also recovered cells from S-phase cell cycle arrest. In addition, both of them promoted the ZEA-induced estrogen production but regulated the expression of steroidogenic enzymes (Star, Cyp11a1, Hsd3b1, Cyp17a1) in different way. All these results indicated that zinc could inhibit the reproductive toxicity of ZEA.
Highlights
Zearalenone (ZEA) mainly injures the reproductive system of mammals
Because zinc and zinc chelator, N,N,N′ N′ -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN), can both be toxic to cells, we determined the optimal concentrations of these substances for subsequent experiments by performing a CCK8 assay
All of the treatments caused a decrease in the cell viability in a dose-dependent manner (Fig. 1A–C), which indicated that both zinc overload and zinc depletion induce the death of KK-1 cells
Summary
Zearalenone (ZEA) mainly injures the reproductive system of mammals. In the present study, we aimed to explore the mechanism by which zinc inhibits ZEA-induced reproductive damage in KK-1 cells for the first time. Zinc recovered cells from S-phase cell cycle arrest Both of them promoted the ZEAinduced estrogen production but regulated the expression of steroidogenic enzymes (Star, Cyp11a1, Hsd3b1, Cyp17a1) in different way. All these results indicated that zinc could inhibit the reproductive toxicity of ZEA. The addition of nutrients to contaminated foods is one approach that reduces the toxicity of mycotoxins. Antioxidants, such as N-acetyl cysteine, vitamins C and E, have been reported to protect animals and cultured cells against the toxic effects of the T-2 toxin and ZEA5–7. Other studies have shown that growth hormones and thymic hormones were affected by zinc supplementation or zinc deficiency[10,11]
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