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Partial cDNA sequence coding for Microtus brandti radde (Brandt's vole) testes-specific lactate dehydrogenase (brLDH-C4) was amplified by reverse transcription-polymerase chain reaction (RT-PCR). By inserting the product into the eukaryotic expression vector pCR3.1, pCR3.1-brLDH-C4 0 was obtained as the prototype of contraceptive DNA vaccine. Immunization with pCR3.1-brLDH-C4 0 in BALB/c mice generated antibodies specific to purified brLDH-C4 0 and native mouse LDH-C4 protein. The birth rate of the pCR3.1-brLDH-C4 0 immunized mice was found to be decreased significantly (80% lower than that of those immunized with pCR3.1). Functions of the elicited antibodies in sera from pCR3.1-brLDH-C4 0 inoculated mice were further explored. The results indicated that the antibodies from the mice injected with pCR3.1-brLDH-C4 0 could cause the agglutination of normal sperm suspension, while the ovarian structure and the development of ovarian follicles of these mice were not impaired, which gives a possible explanation for the immunocontraceptive effects of the pCR3.1-brLDH-C4 0 DNA vaccine.

This study aimed to explore the potential mechanism by which sulfasalazine (SAS) inhibits esophageal cancer cell proliferation. A cell counting kit‐8 (CCK‐8) assay was used to detect the effect of SAS (0, 1, 2, and 4 mM) on the proliferation of TE‐1 cells. Subsequently, TE‐1 cells were divided into control group, SAS group, SAS + ferrostatin‐1 (ferroptosis inhibitor) group, and SAS + Z‐VAD (OH)‐FMK (apoptosis inhibitor) group, and cell proliferation was measured using a CCK‐8 assay. Real‐time quantitative polymerase chain reaction and western blotting were used to determine the expression of solute carrier family member 7 11 (SLC7A11, also called xCT), glutathione peroxidase 4 (GPX4), and acyl‐CoA synthase long‐chain family member 4 (ACSL4) in TE‐1 cells. Measurement of ferroptosis in TE‐1 cells was achieved by flow cytometry. Compared with the control group (0 mM SAS), the proliferation of TE‐1 cells was significantly inhibited by different concentrations of SAS for different time lengths, and 4 mM SAS treatment for 48 h could obtain the maximum inhibition rate (53.9%). In addition, SAS treatment caused a significant decrease in the mRNA and protein expression of xCT and GPX4, and a significant increase in ACSL4 expression in TE‐1 cells treated with SAS. Flow cytometry results showed that the ferroptosis level was significantly increased after SAS treatment. However, the activation of ferroptosis by SAS was partially eliminated by treatment with ferrostatin‐1 or Z‐VAD (OH)‐FMK. In conclusion, SAS inhibits the proliferation of esophageal carcinoma cells by activating the ferroptosis pathway.

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