Asthenozoospermia is a condition of deficient motility of spermatozoa, and about 27.8% of male infertility results from asthenozoospermia. Its etiology is complex and its pathogenesis is still unclear, and exploring its pathogenesis can help to find effective prevention and treatment strategies. In recent years, with the development of proteomic technologies (two-dimensional electrophoresis, yeast two-hybrid technology, mass spectrum, etc.), many researchers have focused their researches on the study of asthenozoospermia based on proteomics, revealing the differential proteins of asthenozoospermia and the biological pathways that underlie them, providing numerous theoretical support for the mechanistic study of asthenozoospermia. In this review, we focus on the relevant techniques of proteomics and summarize the many achievements made in understanding the differential protein expression, etiology, and mechanism of asthenozoospermia, which will hopefully provide new insights into the diagnosis and treatment of asthenozoospermia. Protein-protein interactions and pathways and metabolic abnormalities provide a promising direction to study sperm motility in asthenozoospermia.

Asthenozoospermia is a condition of deficient motility of spermatozoa, and about 27.8% of male infertility results from asthenozoospermia. Its etiology is complex and its pathogenesis is still unclear, and exploring its pathogenesis can help to find effective prevention and treatment strategies. In recent years, with the development of proteomic technologies (two-dimensional electrophoresis, yeast two-hybrid technology, mass spectrum, etc.), many researchers have focused their researches on the study of asthenozoospermia based on proteomics, revealing the differential proteins of asthenozoospermia and the biological pathways that underlie them, providing numerous theoretical support for the mechanistic study of asthenozoospermia. In this review, we focus on the relevant techniques of proteomics and summarize the many achievements made in understanding the differential protein expression, etiology, and mechanism of asthenozoospermia, which will hopefully provide new insights into the diagnosis and treatment of asthenozoospermia. Protein-protein interactions and pathways and metabolic abnormalities provide a promising direction to study sperm motility in asthenozoospermia.

Objective To investigate the effect of low dose of BDE209 on thyroid hormone and thyroid hormone metabolism enzyme-iodothyroninedeiodinases Ⅱ(D2) in off spring mice after pregnancy exposure .Methods Total 64 adult SPF female Kun-ming mice were randomly divided into 4 groups ,which treated with oral gavage of 0 ,50 ,100 ,300 μg · kg -1 · d-1 dose of BDE209 after successful pregnancy ,the exposure continue to 21 days after delivery .10 mice was randomly selected in each offspring group and get the peripheral blood and brain sample ,the serum thyroid hormones level ,oxidative damage and the expression of D2 mRNA in brain were detected .Results Compared with the control group(0μg · kg -1 · d-1 dose of BDE209) ,the TT4 ,TT3 ,FT4 and FT3 levels of offspring mice increased significantly in every exposure group (P< 0 .05);antioxidant enzyme glutathione-S transferees (GST) ,superoxide dismutase (SOD) activity decreased with the BDE209 dose increase (P<0 .05) ,and malondialdehyde (MDA) level increased (P<0 .05);the D2 mRNA relative expression of brain in middle(100μg · kg -1 · d-1 dose of BDE209) and high(300μg · kg -1 · d-1 dose of BDE209) dose group decreased when compared with control group (P< 0 .05) .Conclusion Low level of BDE209 exposure in pregnancy resulted in the increasing of thyroid hormone levels in offspring mice ,which may cause oxidative damage and decrease expression of D2 mRNA in the brain .

OBJECTIVE: To observe the effects of maternal low-level decabromodiphenyl( BDE209) exposure on nervous system and secretion of thyroid hormones in offspring mice. METHODS: Sixty-four specific pathogen free female,aged 4 weeks Kunming mice were used. These mice were randomly divided into control group and low,medium and high exposure groups after successful mating was confirmed. The rats of control group were fed with 0. 01 L/kg body mass of peanut oil.The maternal mice in the experimental groups were given BDE209 at doses of 50,100 and 300 μg/kg body mass by oral gavage once per day. Continuous exposure was given until 21 days after birth of offspring,the exposure model from gestation to lactation was established. At the end of the exposure,10 mice of each group including half female and half male were randomly selected and the body mass and growth development status were observed. Morris water maze was used to examine the learning and memory ability in offspring mice. The serum levels of total triiodothyronine( TT3),free triiodothyronine( FT3), total tetraiodothyronine( TT4) and free tetraiodothyronine( FT4) were measured by chemiluminescence immunoassay. The levels of glutathione transferase( GST), superoxide dismutase( SOD) and malondialdehyde( MDA) level in hippocampus were measured by colorimetry. RESULTS: The escape latency of the medium exposure group was longer than that of the control group( P < 0. 05). The escape latency of high exposure group was longer than that of control group,low exposure group and medium exposure group( P < 0. 05). The time of quadrant movement and number of crossing the platform in offspring rats in high exposure group were less than that of the control group and the low and medium exposure groups( P < 0. 05). The serum levels of TT3,FT3,TT4 and FT4 increased,the activities of GST and SOD in hippocampus tissue decreased,the MDA level increased with the increasing exposure dose( P < 0. 05).CONCLUSION: Maternal low-level BDE209 exposure can result in decrease the learning and memory ability of offspring mice. It also can increase the serum thyroid hormone level and induce oxidative stress injury in hippocampus in a dose dependent manner in offspring mice.

Objective To investigate the joint action of benzene and formaldehyde for oxidative damage effects on cultured CHL cells.Methods Twenty-four hours after the cultured CHL cells exposed to formaldehyde(0,0,0,0.319 75,0.319 75,0.319 75,0.639 5,0.639 5,0.639 5 ?g/ml) or(and) benzene(0,0.392,0.784,0,0.392,0.784,0,0.392,0.784 mg/ml),the level of glutathione(GSH),malondialdehyde(MDA) and the activity of superoxide dismutase(SOD) were determined.Results Twenty-four hours after formaldehyde or(and) benzene exposure,the level of GSH reduced,activity of SOD reduced significantly(P

Objective To explore the combined toxicity of dominant volatile organic compounds(VOCs) and ammonia in indoor air of newly decorated rooms.Methods The gaseous mixture of several main components of VOCs and ammonia was prepared using their pure chemical reagents based on the percentage of mass proportion to each pollutant calculated by the medians of concentrations of formaldehyde,benzene,methylbenzene,dimethylbenzene,ethylbenzene and ammonia obtained from the in situ monitoring data on indoor air of 45 newly decorated apartments.The Kunming mice were exposed to the prepared gaseous mixture at doses of 3.93,8.47,18.24 and 39.35 g/m3 for acute toxicity test,and at doses of 3.935 g/m3(higher dose),1.970 g/m3(middle dose)and 0.393 g/m3(lower dose)for sub-acute toxicity test respectively.Results The LC50 of the prepared gaseous mixture was 26.84 g/m3 for Kunming mice.The sub-acute toxicity test showed that the lower levels of reticulocyte count of female mice in each dose group,the lower level of HCT of female mice dose group,the lower levels of PLT in serum of female and male mice in higher dose group,higher activity of ALT in serum of female mice in higher dose group showed significant differences compared with those of controls (P