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Benzophenone‐3 (BP‐3), one of the most commonly utilized ultraviolet filters in personal care products, has aroused public concern in recent years for its high chances of human exposure. Previous studies have found that BP‐3 can impair testes development and spermatogenesis, but the targets of BP‐3 are still unknown. In this study, primary Sertoli cells from 20‐day‐old mice were treated in vitro with 0–100 μM BP‐3 for 24 h to identify its toxicity on Sertoli cells and Sertoli cell barrier. Results demonstrated that BP‐3 could induce a notable change in cell morphology and impair Sertoli cell viability. The analysis of transepithelial electrical resistance showed that the integrity of the Sertoli cell barrier was destroyed by BP‐3 (100 μM). Some structural proteins of the barrier including ZO‐1, Occludin, and Connexin43 were lower expressed and the localization of basal ectoplasmic specializations protein β‐catenin was altered because of BP‐3 treatment. Further exploration suggested that BP‐3 led to Sertoli cell F‐actin disorganization by affecting the expression of Rictor, a key component of the mTORC2 complex. Moreover, although increased DNA damage marker γH2A.X was observed in the treatment group, the cell apoptosis rate was changeless which was further confirmed by increased BAX and stable Bcl‐2 (two primary apoptosis regulating proteins). In conclusion, this study revealed that BP‐3 had the potential to perturb the Sertoli cell barrier through altered junction proteins and disorganized F‐actin, but it could hardly evoke Sertoli cell apoptosis. [ABSTRACT FROM AUTHOR]

The objective of this study was to examine the efficacy and safety of a novel inhibin vaccine containing inhibin α (1-32) fragments in mice. A recombinant plasmid pVAX-asd-IS was constructed by inserting recombinant inhibin α (1-32) and the hepatitis B surface antigen S into the plasmid in which the asd gene, rather than the kanamycin gene, was a selection marker. Ninety Kuming mice were divided into six groups consisting of 15 mice each. First group was (C1) injected with 200 µl of PBS, second (C2) received 1 × 1010 CFU of crp −/ asd − C500/pVAX-asd and served as vector control, third did not receive any treatment (C3), while fourth, fifth, and sixth group received 1 × 1010, 1 × 109, 1 × 108 CFU of the recombinant inhibin vaccine crp −/ asd − C500/pVAX-asd-IS (group T1, T2, T3), respectively. Western blotting demonstrated that recombinant expressed inhibin protein possessed immune function and that this plasmid could replicate for up to 40 generations stably. Vaccination with this strain at a dose of 1 × 1010 CFU/200 µl per mouse induced high anti-inhibin antibody levels, significantly increased large-follicle production in T1 group ( p < 0.05) and average litter size ( p > 0.05) compared with control groups. Integration studies showed no evidence of inhibin fusion gene integrated into mice's genome 2-month after immunization. These results suggest that the vaccine described in the present study may provide a safe method to improve reproductive traits in animals. A trend towards increased litter size and significant increase in large follicle population depict that this vaccine may have direct application in large animal industry. [ABSTRACT FROM AUTHOR]

Abstract: Cinnamaldehyde is a well-established natural antimicrobial compound. It is probable for cinnamaldehyde to react with amino acid forming Schiff base adduct in real food system. In this paper, 9 such kind of adducts were prepared by the direct reaction of amino acids with cinnamaldehyde at room temperature. Their antimicrobial activities against Bacillus subtilis, Escherichia coli and Saccharomyces cerevisiae were evaluated with benzoic acid as a reference. The adducts showed a dose-dependent activities against the three microbial strains. Both cinnamaldehyde and their adducts were more active against B. subtilis than on E. coli, and their antimicrobial activities were higher at lower pH. Both cinnamaldehyde and its adducts were more active than benzoic acid at the same conditions. The adduct compound A was non-toxic by primary oral acute toxicity study in mice. However, in situ effect of the adduct compound A against E. coli was a little lower than cinnamaldehyde in fish meat. This paper for the first time showed that the cinnamaldehyde adducts with amino acids had similar strong antimicrobial activities as cinnamaldehyde, which may provide alternatives to cinnamaldehyde in food to avoid the strong unacceptable odor of cinnamaldehyde. [Copyright &y& Elsevier]

Gossypol is a yellow natural polyphenolic compound extracted from the seeds, leaves, stems, and flower buds of the cotton plant. Several studies have shown that exposure to gossypol impacts reproductive health in both humans and animals. However, whether gossypol exposure would influence oocyte quality has not yet been determined. Here, we studied the effects of gossypol on the meiotic maturation of mouse oocytes in vitro. The results revealed that gossypol exposure did not affect germinal vesicle breakdown (GVBD) but significantly reduced polar body extrusion (PBE) rates. Moreover, we observed meiotic spindle organization and chromosome alignment were entirely disturbed after gossypol exposure. Further, gossypol exposure also caused mitochondrial dysfunction and abruptly decreased the levels of cellular ATP, and diminished the mitochondrial membrane potential (MMP). Accordingly, gossypol-induced oxidative stress was confirmed through an increased level of reactive oxygen species (ROS). Early apoptosis incidence also increased as identified by positive Annexin-V signaling. Collectively, the above findings provide evidence that gossypol exposure impaired oocyte meiotic maturation, disturbed spindle structure and chromosome dynamics, disrupted mitochondrial function, induced oxidative stress, and triggered early apoptosis. These findings emphasize gossypol's adverse effects on oocyte maturation and thus on female fertility. • Gossypol exposure compromised the meiotic maturation of mouse oocytes. • Gossypol exposure disturbed the spindle assembly and chromosome alignment. • Gossypol exposure caused mitochondrial damage and reduced ATP content and MMP. • Gossypol exposure increased ROS level in mouse oocytes. • Gossypol exposure induced early apoptosis in mouse oocytes. [ABSTRACT FROM AUTHOR]