Pubertal exposure to acrylamide disrupts spermatogenesis by interfering with meiotic progression in male mice.

Teenagers are a major group likely to love junk foods, such as potato chips and bread items, which contain high levels of acrylamide (AA). The increasing evidence suggests that AA exposure may be associated with decreased reproductive capacity in humans and animals. However, the reproductive toxicity of AA in pubertal males has not been fully elucidated. In this study, we evaluated the effects of pubertal AA exposure on adult spermatogenesis in male mice. Mice were exposed to AA at 0, 5, 10, 20, and 40 mg/kg/day by gavage from postnatal day 28 (PND28) to PND56. Our results showed that pubertal AA exposure increased apoptosis of germ cells in seminiferous tubules, decreased sperm concentration, and caused defects in sperm of adult mice. To explore the possible mechanisms of AA on spermatogenesis, the meiotic process was analyzed. The ratio of leptotene and zygotene spermatocytes increased, while the pachytene and diplotene spermatocytes decreased in AA-treated mice. Further analysis revealed that AA exposure disrupted the pattern of H2AX phosphorylation expansion, synapsis, and the crossover formation during meiotic prophase I (MPI). Taken together, these results indicate that pubertal AA exposure affects the spermatogenesis may be by disrupting the MPI progression of male mice.

Acrylamide impairs the developmental potential of germinal vesicle oocytes by inducing mitochondrial dysfunction and autophagy/apoptosis in mice.

Background: Acrylamide (ACR), an important endogenous contaminant in carbohydrate-rich foods, has been involved in various negative effects on multiple organ networks, including the reproductive system. Previous studies have reported that ACR affects oocyte quality and fertility. Purpose: This study aimed to explore the toxic effects and regulatory mechanisms of ACR on mouse germinal vesicle (GV) oocytes. Research Design: In this study, adult female mice were exposed to ACR at 10 mg/kg/day/body weight through their drinking water continuously for 4 weeks. Study Sample and Data Analysis: The mitochondrial function, autophagy/apoptosis, and development potential of GV oocytes were investigated. Results: The results showed that ACR reduced the oocyte diameter, sperm-binding ability, parthenogenetic activation and in vitro fertilization (IVF) rate, and development potential of pre-implantation embryos. We also found that ACR exposure disrupted chromatin configuration, mitochondrial distribution, and membrane potential (Δφm) of oocytes. Actin filament expression was significantly reduced in both the membrane and cytoplasm of mouse oocytes. Moreover, ACR exposure increased LC3-positive signals, early apoptosis rate, aberrant ATG3, ATG5, LC3, Beclin1, and mTOR mRNA expression. Conclusions: These results suggest that ACR exposure can affect the developmental potential of GV oocytes by inducing mitochondrial dysfunction, actin filament assembly, and autophagy/apoptosis.

[Atrazine changes meiosis and reduces spermatogenesis in male mice].

OBJECTIVE: To investigate the effects of exposure to atrazine on meiosis and spermatogenesis in adult male mice. METHODS: We divided 16 adult male Institute for Cancer Research (ICR) mice into a solvent control and an atrazine exposure group of an equal number and intraperitoneally injected with solvent dimethylsulfoxide (DMSO) and atrazine at 100 mg/kg/d, respectively. After 4 weeks of treatment, we obtained the body and testis weights of the mice, observed the changes in the testicular histomorphology, examined the cell apoptosis in the testis tissue, and determined the expressions of meiosis-related key genes in the spermatocytes by real-time fluorescence quantitative PCR. RESULTS: Compared with the controls, the mice treated with atrazine showed significantly less increase in the body weight (ï¼»11.2 ± 0.17ï¼½ vs ï¼»8.29 ± 0.51ï¼½ g, P < 0.05) and testis weight (ï¼»0.28 ± 0.01ï¼½ vs ï¼»0.24 ± 0.01ï¼½ g, P < 0.05), loosely arranged and thinned lumens of seminiferous tubules, disordered arrangement and reduced number of spermatogenic cells, decreased sperm concentration (ï¼»2.36 ± 0.14ï¼½ vs ï¼»0.90 ± 0.12ï¼½ ×106/ml, P < 0.01) and increased percentage of morphologically abnormal sperm in the epididymis tail (ï¼»8.60 ± 1.07ï¼½% vs ï¼»18.02 ± 1.71ï¼½%, P < 0.05), elevated apoptosis rate of spermatocytes, and down-regulated the expressions of SCP1, SCP3 and Rad51 mRNA in the spermatocytes (P < 0.05). CONCLUSIONS: Atrazine can reduce spermatogenesis in male mice by damaging testicular morphology, increasing the apoptosis of spermatocytes and down-regulating the expressions of meiosis-related genes in the spermatocytes.

[Adaptive evolution of the hemagglutinin genes of the H6N1 avian influenza virus in Taiwan, China].

In Taiwan, the first human-infecting H6N1 avian influenza virus was isolated in 2013. To better understand the origin, evolutionary relationship and pathogenesis of the H6N1 virus, we studied the adaptive evolution and evolutionary dynamics of the hemagglutinin (HA) genes of the H6N1 virus in Taiwan. We felt that such studies woud contribute to the further study and control of the virus. Datasets were gained from the Flu and Global Initiative on Sharing All Influenza Data (GISAID) databases. Then, phylogenetic trees and evolutionary dynamics were reconstructed. The evolutionary rate and characterization of adaptive evolution were analyzed by bioinformatic methods. Results indicated that the HA genes of H6N1 in Taiwan were divided into at least five types, and that the new types that the infected human H6N1 belonged to could be local advantage type at present. Evolutionary dynamics revealed the viral population expanded first at the end of 1971, reduced sharply in 2008, and then increased slightly. Three sites were identified under positive selection, suggesting that various sites might increase the adaptive ability of the virus. Eighty-nine sites were under negative selection, revealing that these sites might play an important role in the replication and epidemiology of the virus. Interestingly, site 329 upstream from the cleavage site was also under negative selection, suggesting that this site might be associated with the virulence of H6N1. These data suggest that the HA genes of the Taiwanese H6N1 virus have been undergoing adaptive evolution, and that an outbreak may occur again. Hence, more attention should be paid to the identified sites, to enable timely monitoring and control of a future epidemic.