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The liver is an organ that is particularly exposed to reactive oxygen species (ROS), which not only arise during metabolic functions but also during the biotransformation of xenobiotics. The disruption of redox balance causes oxidative stress, which affects liver function, modulates inflammatory pathways and contributes to disease. Thus, oxidative stress is implicated in acute liver injury and in the pathogenesis of prevalent infectious or metabolic chronic liver diseases such as viral hepatitis B or C, alcoholic fatty liver disease, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Moreover, oxidative stress plays a crucial role in liver disease progression to liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Herein, we provide an overview on the effects of oxidative stress on liver pathophysiology and the mechanisms by which oxidative stress promotes liver disease. [ABSTRACT FROM AUTHOR]

DNA repair is an important pathway for the protection of DNA molecules from destruction. DNA damage can be produced by oxidative reactive nitrogen or oxygen species, irritation, alkylating agents, depurination and depyrimidination; in this regard, DNA repair pathways can neutralize the negative effects of these factors. Melatonin is a hormone secreted from the pineal gland with an antioxidant effect by binding to oxidative factors. In addition, the effect of melatonin on DNA repair pathways has been proven by the literature. DNA repair is carried out by several mechanisms, of which homologous recombination repair (HRR) and non‐homologous end‐joining (NHEJ) are of great importance. Because of the importance of DNA repair in DNA integrity and the anticancer effect of this pathway, we presented the effect of melatonin on DNA repair factors regarding previous studies conducted in this area. [ABSTRACT FROM AUTHOR]

Introduction: P53, as a tumor suppressor gene, is believed to be one of the most mutated genes in cancer cells. The mutant forms of this protein often play a tumorigenic role in cancer cells. Recent evidence shows that p53 plays a critical role in the migration, metastasis, and invasion of cancer cells. The present article aims to investigate the molecular mechanism that induces metastasis in cancer cells generated by the mutant P53, and to highlight the compounds targeting mutant-p53 together with their clinical applications. Methods: A detailed literature search was conducted to find information about the role of the mutant-p53 in the processes involved in metastasis in various databases. Results: A growing body of evidence suggests that Mutant-p53 enhances tumor metastasis affecting the Epithelial-mesenchymal transition (EMT) process, cancer stem cells, angiogenesis, autophagy, anoikis, and any other mechanisms regarding metastasis. Conclusions: Taken together, targeting mutant-p53 by altering the processes involved in metastasis could be a potential therapeutic strategy in the treatment of metastatic cancer. [ABSTRACT FROM AUTHOR]

Objective: Oxidative stress plays a key role in the pathogenesis of male infertility. But, the adverse effects of oxidative biomarkers on sperm quality remain unclear. This study aimed to investigate the levels of nitric oxide (NO), 8-hydroxydesoxyguanosine (8-OHdG), and total antioxidant capacity (TAC) oxidative biomarkers in seminal plasma and their relationship with sperm parameters. Methods: A total of 77 volunteers participated in the study, including fertile (n=40) and infertile men (n=37). NO, 8-OHdG, and TAC levels were measured using the ferric reducing ability of plasma, Griess reagent method and an enzyme-linked immunosorbent assay kit, respectively. Results: The mean values of sperm parameters in the infertile group were significantly lower than those in the fertile group (p<0.001). The mean 8-OHdG in the seminal plasma of infertile men was significantly higher (p=0.013) than those of controls, while the mean TAC was significantly lower (p=0.046). There was no significant difference in NO level between the two groups. The elevated seminal 8-OHdG levels were negatively correlated with semen volume, total sperm counts and morphology (p<0.001, p=0.001 and p=0.052, respectively). NO levels were negatively correlated with semen volume, total sperm counts and morphology (p=0.014, p=0.020 and p=0.060, respectively). Positive correlations between TAC and both sperm count and morphology (p=0.043 and p=0.025, respectively) were also found. Conclusion: These results suggested that increased levels of NO and 8-OHdG in seminal plasma could have a negative effect on sperm function by inducing damage to the sperm DNA hence their fertility potentials. Therefore, these biomarkers can be useful in the diagnosis and treatment of male infertility. [ABSTRACT FROM AUTHOR]

Background and objectives: 3' untranslated region (3'UTR) single nucleotide polymorphisms (SNPs) represent genetic variations that may potentially affect binding of miRNA to coding genes, potentially leading to complex disorders. We aimed to perform in silico analysis of the potential phenotypic effect of 3'UTR SNPs on human astrocyte elevated gene-1 (AEG-1), a newly identified candidate cancer gene. Methods: We gathered a list of all 3'UTR SNPs located in the human AEG-1 gene from the SNP database. Analysis of the potential effects was done using MirSNP and MicroSNiper. Results: Analysis by the MirSNP estimated that rs187728237 might increase the affinity of two miRNAs and decrease the affinity of 10 other miRNAs to the AEG-1 transcript. Moreover, MicroSNiPer showed that rs80320514 might affect 24 putative miRNA binding sites in the 3'UTR of AEG-1. Conclusion: Based on our findings, it can be concluded that the 3'UTR SNPs located in the human AEG-1 gene may be within the miRNA targets of the transcript, therefore affecting the stability of putative miRNA-target interactions. [ABSTRACT FROM AUTHOR]