Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

Recent genomic studies have identified novel recurrent somatic mutations in patients with myeloid malignancies, including myeloproliferative neoplasms (MPNs), myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML). In some cases these mutations occur in genes with known roles in regulating chromatin and/or methylation states in haematopoietic progenitors, and in other cases genetic and functional studies have elucidated a role for specific mutations in altering epigenetic patterning in myeloid malignancies. In this Review we discuss recent genetic and functional data implicating mutations in epigenetic modifiers, including tet methylcytosine dioxygenase 2 (TET2), isocitrate dehydrogenase 1 (IDH1), IDH2, additional sex combs-like 1 (ASXL1), enhancer of zeste homologue 2 (EZH2) and DNA methyltransferase 3A (DNMT3A), in the pathogenesis of MPN, MDS and AML, and discuss how this knowledge is leading to novel clinical, biological and therapeutic insights.

The role of mutations in epigenetic regulators in myeloid malignancies

https://www.abc.es/gestordocumental/uploads/Sociedad/Sakkas%20Alvarez%20FS.pdf

Sperm DNA fragmentation: mechanisms of origin, impact on reproductive outcome, and analysis

Histone posttranslational modifications represent a versatile set of epigenetic marks involved not only in dynamic cellular processes, such as transcription and DNA repair, but also in the stable maintenance of repressive chromatin. In this article, we review many of the key and newly identified histone modifications known to be deregulated in cancer and how this impacts function. The latter part of the article addresses the challenges and current status of the epigenetic drug development process as it applies to cancer therapeutics.

/pdf/histone-modifications-and-cancer-w2boj1xl6t.pdf

Histone Modifications and Cancer.

Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.

/pdf/impacts-of-oxidative-stress-and-antioxidants-on-semen-4jjpffmz38.pdf

Impacts of Oxidative Stress and Antioxidants on Semen Functions

https://www.clevelandclinic.org/reproductiveresearchcenter/docs/agradoc387.pdf

TUNEL as a test for sperm DNA damage in the evaluation of male infertility

https://www.clevelandclinic.org/reproductiveresearchcenter/docs/agradoc357.pdf

Semen characteristics and sperm DNA fragmentation in infertile men with low and high levels of seminal reactive oxygen species

https://www.fertstert.org/article/S0015-0282(08)00003-4/pdf

Diagnostic value of the total antioxidant capacity (TAC) in human seminal plasma.

https://www.clevelandclinic.org/reproductiveresearchcenter/docs/agradoc382.pdf

Sperm viability, apoptosis, and intracellular reactive oxygen species levels in human spermatozoa before and after induction of oxidative stress

https://www.clevelandclinic.org/reproductiveresearchcenter/docs/agradoc349.pdf

Reda Z. Mahfouz

Papers

TUNEL as a test for sperm DNA damage in the evaluation of male infertility

Semen characteristics and sperm DNA fragmentation in infertile men with low and high levels of seminal reactive oxygen species

Diagnostic value of the total antioxidant capacity (TAC) in human seminal plasma.

Sperm viability, apoptosis, and intracellular reactive oxygen species levels in human spermatozoa before and after induction of oxidative stress

L-Carnitine decreases DNA damage and improves the in vitro blastocyst development rate in mouse embryos