No abstract

The human gut microbiota has a significant effect on many aspects of human physiology such as metabolism, nutrient absorption, and immune function. Imbalance of the microbiota has been implicated in many disorders including inflammatory bowel disease, obesity, asthma, psychiatric illnesses, and cancers. As a kind of functional foods, probiotics have been shown to play a protective role against cancer development in animal models. Clinical application of probiotics indicated that some probiotic strains could diminish the incidence of postoperative inflammation in cancer patients. Chemotherapy or radiotherapy-related diarrhea was relieved in patients who were administered oral probiotics. The present review summarizes the up-to-date studies on probiotic effects and the underlying mechanisms related to cancer. At present, it is commonly accepted that most commercial probiotic products are generally safe and can improve the health of the host. By modulating intestinal microbiota and immune response, some strains of probiotics can be used as an adjuvant for cancer prevention or/and treatment.

Irrigation in semiarid regions can alter soil C sequestration processes compared with those of native soils. To better understand the effect of these altered processes, we studied the C sequestration and dynamics of two soils from major irrigated agricultural regions of California (the San Joaquin Valley and the Imperial Valley). Soils were sampled from selected native and cultivated fields to represent a span of almost a century of irrigated farming. Field soil samples were analyzed for total soil C and soil inorganic C as carbonate (SIC). Soil organic C (SOC) was then calculated from the measured data. Results showed that SOC stock increased above that stored in the native soil after five decades of irrigated farming. The SIC stock showed opposing trends within the top meter of the two studied soils: a decrease was measured after 55 yr in the San Joaquin Valley soil, while SIC in the Imperial Valley soil increased after 85 yr of irrigated agriculture and appears to represent a significant form of sequestered soil C. Our results indicate that long‐term irrigated farming can significantly increase SOC due primarily to SOC added below the 10‐cm soil depth, while significant increases in SIC may be partially due to the conversion of increased soil CO2 to carbonates under a regime of Colorado River irrigation water. Thus, when considering C sequestration in irrigated agriculture in semiarid regions, it is important to determine levels of both SOC and SIC.

As a persistent organic pollutant, microplastics (MPs) have been reported to induce sperm quantity decrease in male rats. However, the related mechanism remains obscure. Therefore, this study is intended to explore the effects of polystyrene microplastics (PS-MPs) on male reproduction and its related mechanism of blood-testis barrier (BTB) impairment. Thirty-two adult male Wistar rats were divided randomly into four groups fed with PS-MPs for 90 days at the dose of 0 mg/d (control group), 0.015 mg/d, 0.15 mg/d and 1.5 mg/d respectively. The present results have showed that PS-MPs exposure led to the damage of seminiferous tubule, resulted in apoptosis of spermatogenic cell and decreased the motility and concentration of sperm, while the abnormality of sperm was elevated. Meanwhile, PS-MPs could induce oxidative stress and activate p38 MAPK pathway and thus deplete the nuclear factor erythroid-2 related factor 2 (Nrf2). Noteworthily, the adverse effect of PS-MPs on BTB is only signi cant in 0.15 mg/d and 1.5 mg/d groups ,which demonstrated that high-dose PS-MPs exposure may lead to the destruction of BTB integrity and the apoptosis of spermatogenic cells through the activation of MAPK-Nrf2 pathway. The current study provided novelty evidence for elucidating the effects of PS-MPs on male reproductive toxicity and its potential mechanism.

We observed frequent stillbirth in peroxiredoxin III (PrxIII) knockout maternal mice. Quantitative real time PCR (qRT-PCR) and Western-blot analysis revealed increased oxidative stress in placentas that were deficient in PrxIII. We did not find significant difference between PrxIII knockout maternal mice and wild-type littermates in hematological parameters, fetal number, and embryonic development. Nevertheless, we noticed enhanced expression of PrxI in erythrocytes of pregnant knockout mice. Our results provided in vivo evidence that PrxIII played a crucial role in placental antioxidant defense. Up-regulation of PrxI might provide a compensation that protected erythrocytes against oxidative damage.

Abstract. Although peroxiredoxin 3 (Prx3) has been reported to be involved in cervical cancer (CC) carcinogenesis, the significance of Prx3 in CC progression remains unclear. The present study was conducted to investigate the expression features of Prx3 to better understand the mechanism of tumor growth and invasion. Sixty-eight patients with invasive squamous cervical cancer were included in the present study. The status of human papillomavirus (HPV) infection was detected by hybridization and quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemistry was performed on paraffin-embedded sections using monoclonal antibodies against Prx3 and Ki67. All samples were positive for high-risk HPV, among which fifty-six samples were positive for HPV16, seven for HPV18 and five for HPV33. The expression of HPV16 E6/E7 was significantly higher in cancer areas compared to the adjacent normal epithelial tissuses. The positive cells for Prx3 and Ki67 were significantly higher in cancer cells compared to normal epitheliums and the staining pattern of Prx3 was consistent with that of Ki67 (Pearson's correlation coefficient was 0.801, P= 0.000). The upregulation of Prx3 might be a protective response to oxidative stress in the cancer microenvironment. The expression consistency of Prx3 and Ki67 suggests Prx3 to be a potential marker for cell proliferation of CC.

Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers.

High-risk human papillomavirus (HPV) type 16, which is responsible for greater than 50% of cervical cancer cases, is the most prevalent and lethal HPV type. However, the molecular mechanisms of cervical carcinogenesis remain elusive, particularly the early steps of HPV infection that may transform normal cervical epithelium into a pre-neoplastic state. Here, we report that a group of microRNAs (microRNAs) were aberrantly decreased in HPV16-positive normal cervical tissues, and these groups of microRNAs are further reduced in cervical carcinoma. Among these miRNAs, miR196a expression is the most reduced in HPV16-infected tissues. Interestingly, miR196a expression is low in HPV16-positive cervical cancer cell lines but high in HPV16-negative cervical cancer cell lines. Furthermore, we found that only HPV16 early gene E5 specifically down-regulated miRNA196a in the cervical cancer cell lines. In addition, HoxB8, a known miR196a target gene, is up-regulated in the HPV16 cervical carcinoma cell line but not in HPV18 cervical cancer cell lines. Various doses of miR196a affected cervical cancer cell proliferation and apoptosis. Altogether, these results suggested that HPV16 E5 specifically down-regulates miR196a upon infection of the human cervix and initiates the transformation of normal cervix cells to cervical carcinoma.