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Background: Oligohydramnios presents a threat to the fetus and has been correlated with increased risk of intrauterine growth retardation, meconium aspiration syndrome, severe birth asphyxia, low APGAR scores and congenital abnormities. It is associated with perinatal morbidity and mortality and maternal morbidity in a significant number of cases. Therefore, early detection of oligohydramnios and its management is important. Aim of this study was to know the fetal and maternal outcome in oligohydramnios.Methods: 90 patients in third trimester of pregnancy with Oligohydramnios were selected after satisfying inclusion and exclusion criteria. A detailed history and examination were done. All required investigation done. Oligohydramnios confirmed by measuring Amniotic fluid index (AFI).Results: Mean maternal age-26.1 years. Incidence of oligohydramnios was more in primipara (64.4%) in our study. And operative morbidity was also more in primipara (51.7%). Most common cause of Oligohydramnios was idiopathic (44.44%). Operative morbidity was significantly higher in Non-reassuring FHR (80%) than reassuring FHR (32%). 7 patients (7.78%) were found with fetoplacental insufficiency on Doppler study.Conclusions: Oligohydramnios is frequent occurrence and demands intensive fetal surveillance and proper antepartum and intrapartum care so that perinatal morbidity and mortality and maternal morbidity can be reduced.

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Graphical abstract The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational events are considered the major triggers for introducing genetic and epigenetic insults such as DNA crosslinks, single- and double-strand DNA breaks, formation of DNA adducts, mismatched bases, modification in histones, DNA methylation, and microRNA alterations. However, DNA repair mechanisms are devoted to protect the DNA to ensure genetic stability, any aberrations in these calibrated mechanisms provoke cancer occurrence. Comprehensive knowledge of the type of mutagens and carcinogens and the influence of these agents in DNA damage and cancer induction is crucial to develop rational anticancer strategies. This review delineated the molecular mechanism of DNA damage and the repair pathways to provide a deep understanding of the molecular basis of mutagenicity and carcinogenicity. A relationship between DNA adduct formation and cancer incidence has also been summarized. The mechanistic basis of inflammatory response and oxidative damage triggered by mutagens in tumorigenesis has also been highlighted. We elucidated the interesting interplay between DNA damage response and immune system mechanisms. We addressed the current understanding of DNA repair targeted therapies and DNA damaging chemotherapeutic agents for cancer treatment and discussed how antiviral agents, anti-inflammatory drugs, and immunotherapeutic agents combined with traditional approaches lay the foundations for future cancer therapies.