Fluoride and sulfur dioxide are two well known environment pollutants, co-existing in some places, which present a serious threat to public health. In order to explore the potential toxic effects of the two pollutants on the male reproduction and the mechanism of their interaction, sexually matured rats and unmatured mice were treated with fluoride (100mg/L NaF) and sulfur dioxide (39.3 mg/m³ SO₂, 4hr/day), and fluoride (150mg/L NaF) and sulfur dioxide (26.2mg/m³ SO₂，3hr/day), respectively. Applied diverse methods as radioimmunoassay, transmission electronic microscopic, flow cytometry (FCM) and Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling (TUNEL), immunohidtochemidtry and Real-time PCR, this study dynamically observed the changes of sperm quality, morphology and subcellular structure of testis, protein level, antioxidation and the activity of relative enzymes in testis, apoptosis in seminaferous cell and the expression of p53、bcl-2、bax gene in these two kinds of models. Moreover, miRNA microarray，a new explored technology, was used to examined the changes of non-coded RNA in order to study the mechanism of effects of these two elements on the spermatogenesis. Afterwards, the MAPK pathway（ERK1/2、JNK1/2/3、p38 and ERK5）and transcriptional factors of p38 downstream （GADD153、MAX、MEF2C and Sap1a）expression levels in mice testis were assessed according to the results of bioinformatics’ analysis. The results indicate that sulfur dioxide sharpen the damage of Fluoride on male reproductive system, including the changes in structure of tissues, cell and molecular level so that significantly destroy the reproductive function. The toxic effect of fluoride is in coordination with sulfur dioxide, the mechanism of which may be that fluoride and sulfur dioxide produce oxidative stress in testis tissue, disrupt the DNA single chain, activate DNA-PK, and induce phosphorylation and activation of p53 protein. Furthermore, the activated p53 protein can enhance the expression of apoptosis gene such as bcl-2, bax et al. and start spermatogenic cells apoptosis, finally impair spermiogenesis. Moreover, miRNAs and MAPK signal pathways maybe play the key role during the injure regulation.

Acknowledgements: This research was sponsored by the China National Natural Science Foundation (Grant No. 30671545; 30901092；31172380；31072180), the Specialized Research Fund for the Doctoral Program of Higher Education of China (Grant No. 20091403120002), Natural Science Foundation for Young Scientists of Shanxi Province (Grant No. 2009021035-1), Shanxi Province Provincial Foundation for Leaders of Disciplines in Science (Grant No.201001)..

Authors: Zhang Jian-hai,^a Liang Chen,^a Sun Zi-long,^a Luo Guang-ying, ^a Wang Xiao-wen, ^a Wang Jung-dong^a

Correspondence: ^aProf. Jundong Wang, Shanxi Key Laboratory of Ecological Animal Science and Environmental Medicine, Shanxi Agricultural University, Taigu, Shanxi 030801, P.R. of China.

E-mail: [email protected]

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