Ionizing radiation impairs ovarian function by inducing DNA double-strand breaks, oxidative stress, and inflammatory cascades, leading to primordial follicle depletion and premature ovarian insufficiency (POI). Core mechanisms involve ATM/p53-mediated DNA damage response, granulosa cell apoptosis triggered by a sharp increase in reactive oxygen species/reactive nitrogen species (ROS/RNS), and Toll-like receptor (TLR)/NF-κB-driven chronic inflammation. Currently, only amifostine and palifermin are internationally approved radioprotective agents, yet they exhibit significant limitations including severe toxicity, narrow indications, and lack of conclusive evidence for ovarian protection. Investigational agents like the natural antioxidant melatonin require further clinical validation for ovarian radioprotection. Emerging strategies, such as TLR5 agonists, mitochondrial-targeted agents, and targeted drug delivery systems, provide novel directions for mitigating radiation-induced ovarian injury. This review synthesizes key pathways of radiation-induced ovarian damage, explores cutting-edge mechanisms, and highlights promising novel radioprotective agents. The proposed synergistic “epigenetic regulation + immunomodulation” strategy embodies a paradigm shift from passive mitigation to active precision protection against ovarian radiation damage.

Objective To explore the clinical characteristics and factors affecting the prognosis of metastatic ovarian tumors of gastric and colorectal cancer.Methods Clinical data of 92 hospitalized patients with metastatic ovarian tumors of gastric and colorectal cancer in The First Affiliated Hospital of Naval Medical University from January 2010 to August 2020 were selected and analyzed retrospectively.The clinical characteristics,related laboratory data,survival and prognostic factors were statistically analyzed.Results There were less than half of carcinoembryonic antigen(CEA)-positive cases and less than half of carbolydrate antigen 125(CA125)-positive cases in the 92 cases.Medium-sized solid or cystic solid masses(5-10 cm)mainly presented on imaging.The median survival time of the patients was 16 months,and 1-,2-and 3-year overall survivals were 55.9%,36.8%and 17.6%,respectively.Univariate analysis showed that negative CA125,CA125/CEA<5,colorectal origin,adenocarcinoma of primary tumor,the resection of primary tumor,no external ovarian metastases,no residual of metastatic lesions after surgery,no vascular invasion of ovarian metastases,unilateral ovarian mass,ovarian mass less than 5 cm,ovarian metastases containing cystic components,and adenocarcinoma of ovarian metastases were related to a good prognosis.The expression of caudal type homeobox 2(CDX2)affected the survival time(P=0.001).COX regression multivariate analysis identified that the primary tumor site(P=0.023),ovarian mass<5 cm(P=0.031),and the expression of P53 in ovarian metastasis(P=0.007)were independent prognostic factors for metastatic ovarian tumors of gastric and colorectal cancer.Conclusion There is a wide range of onset age of patients with metastatic ovarian tumors of gastric and colorectal cancer.The clinical manifestations were nontypical,and medium-sized masses containing solid components mainly present on imaging.The prognosis is poor,but the patients with colorectal origin have better prognosis than patients with gastric origin.The prognosis of patients with ovarian mass<5 cm is good.The expression of P53 may be a protective factor for those patients.

The survival rate of cancer patients was improved due to the development of cancer treatment techniques, and thus the fertility protection for young female cancer patients has attracted increasing attention. Radiotherapy, as one of the comprehensive cancer treatment, could cause ovarian damage in adolescent and child-bearing women, which leads to fertility decline and a series of side effects. Radiation can cause ovarian damage not only by acting on biological macromolecules directly, but also by increasing oxidative stress between oocytes and ovarian granulosa cells indirectly. At present, the fertility preservation of female cancer patients undergoing radiotherapy mainly includes physical protection, drug protection and biological protection. Recently, the development of new technologies for the preservation of fertility in female cancer patients has also brought new hope, including factors such as protective effects, patient age, and the selection of specific cancer treatment measures, which are the main considerations in the selection process of fertility preservation measures. This article reviews the research progress on radiation-induced ovarian damage, with a focus on the introduction of the fertility preservation measures and new technologies for young female tumor patients receiving radiotherapy.

Objective:To investigate the role of mitochondrial transcription termination factor domain 1 (MTERFD1) in regulating the malignant biological behavior of ovarian cancer (OC) cells and preliminarily reveal its molecular mechanism.Methods:RT-qPCR was used to detect the expression levels of MTERFD1 mRNA in human OC cell lines SKOV3, HEY, and OVCAR3, human embryonic kidney epithelial cells HEK-293, and normal ovarian tissues. After transfecting these cells with MTERFD1 overexpression plasmid and small interfering RNA, MTT analysis was used to detect the cell proliferation, and Annexin V/PI double staining assay was used to detect apoptosis. ELISA was used to check the effect of MTERFD1 level on the expression of IL-6. MTT analysis was used to evaluate the effect of IL-6 level changing on the proliferation of OC cells with different MTERFD1 expressions.Results:The MTERFD1 mRNA levels in OC cell lines SKOV3, HEY, and OVCAR3 were higher than those in HEK-293 cell line and normal ovarian tissues with statistically significant differences ( P<0.05). In human OC OVCAR3 and HEK-293 cell lines, the cell proliferation in the group of MTERFD1 overexpression plasmid was higher than that in the blank plasmid group; after the MTERFD1 being knocked out, the HEY and SKOV3 cell proliferations obviously decreased and the apoptosis rates were higher than those in the negative control group; all differences were statistically significant ( P<0.05). The IL-6 levels in OC cells were positively correlated with MTERFD1 expressions, and the IL-6 blocking antibody could reverse the promoting effect of MTERFD1 on the proliferation of OC cells. Conclusion:The promoting effect of MTERFD1 on the proliferation of ovarian cancer cells may be achieved through regulating IL-6.

Objective:To investigate the role of mitochondrial transcription termination factor domain 1 (MTERFD1) in regulating the malignant biological behavior of ovarian cancer (OC) cells and preliminarily reveal its molecular mechanism.Methods:RT-qPCR was used to detect the expression levels of MTERFD1 mRNA in human OC cell lines SKOV3, HEY, and OVCAR3, human embryonic kidney epithelial cells HEK-293, and normal ovarian tissues. After transfecting these cells with MTERFD1 overexpression plasmid and small interfering RNA, MTT analysis was used to detect the cell proliferation, and Annexin V/PI double staining assay was used to detect apoptosis. ELISA was used to check the effect of MTERFD1 level on the expression of IL-6. MTT analysis was used to evaluate the effect of IL-6 level changing on the proliferation of OC cells with different MTERFD1 expressions.Results:The MTERFD1 mRNA levels in OC cell lines SKOV3, HEY, and OVCAR3 were higher than those in HEK-293 cell line and normal ovarian tissues with statistically significant differences ( P<0.05). In human OC OVCAR3 and HEK-293 cell lines, the cell proliferation in the group of MTERFD1 overexpression plasmid was higher than that in the blank plasmid group; after the MTERFD1 being knocked out, the HEY and SKOV3 cell proliferations obviously decreased and the apoptosis rates were higher than those in the negative control group; all differences were statistically significant ( P<0.05). The IL-6 levels in OC cells were positively correlated with MTERFD1 expressions, and the IL-6 blocking antibody could reverse the promoting effect of MTERFD1 on the proliferation of OC cells. Conclusion:The promoting effect of MTERFD1 on the proliferation of ovarian cancer cells may be achieved through regulating IL-6.