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Lipid oxidation has long been regarded as a deleterious process responsible for lipid rancidity, loss of function, and generation of toxic products. However in recent years, research has also focused on the non-detrimental physiological and pathological effects of these chemical reactions. This book provides an up-to-date review of the role of oxidized lipid products in physiological and pathophysiological processes. Topics include the mechanisms of lipid oxidation, antioxidant defenses, lipid oxidation products, cell signaling, and the roles of oxidized lipids in specific diseases. The book also discusses drug targeting and the therapeutic potential of oxidized lipids.

Reactive oxygen species (ROS) are continuously produced in living cells due to metabolic and biochemical reactions and due to exposure to physical, chemical and biological agents. Excessive ROS cause oxidative stress and lead to oxidative DNA damage. Within ROS-mediated DNA lesions, 8-oxoguanine (8-oxoG) and its nucleotide 8-oxo-2′-deoxyguanosine (8-oxodG)—the guanine and deoxyguanosine oxidation products, respectively, are regarded as the most significant biomarkers for oxidative DNA damage. The quantification of 8-oxoG and 8-oxodG in urine, blood, tissue and saliva is essential, being employed to determine the overall effects of oxidative stress and to assess the risk, diagnose, and evaluate the treatment of autoimmune, inflammatory, neurodegenerative and cardiovascular diseases, diabetes, cancer and other age-related diseases. High-performance liquid chromatography with electrochemical detection (HPLC–ECD) is largely employed for 8-oxoG and 8-oxodG determination in biological samples due to its high selectivity and sensitivity, down to the femtomolar range. This review seeks to provide an exhaustive analysis of the most recent reports on the HPLC–ECD determination of 8-oxoG and 8-oxodG in cellular DNA and body fluids, which is relevant for health research.

Oxidative DNA damage plays an important role in the pathogenesis of various diseases. Among oxidative DNA lesions, 8-oxoguanine (8-oxoG) and its corresponding nucleotide 8-oxo-2′-deoxyguanosine (8-oxodG), the guanine and deoxyguanosine oxidation products, have gained much attention, being considered biomarkers for oxidative DNA damage. Both 8-oxoG and 8-oxodG are used to predict overall body oxidative stress levels, to estimate the risk, to detect, and to make prognosis related to treatment of cancer, degenerative, and other age-related diseases. The need for rapid, easy, and low-cost detection and quantification of 8-oxoG and 8-oxodG biomarkers of oxidative DNA damage in complex samples, urine, blood, and tissue, caused an increasing interest on electrochemical sensors based on modified electrodes, due to their high sensitivity and selectivity, low-cost, and easy miniaturization and automation. This review aims to provide a comprehensive and exhaustive overview of the fundamental principles concerning the electrochemical determination of the biomarkers 8-oxoG and 8-oxodG using nanostructured materials (NsM), such as carbon nanotubes, carbon nanofibers, graphene-related materials, gold nanomaterials, metal nanoparticles, polymers, nanocomposites, dendrimers, antibodies and aptamers, and modified electrochemical sensors. Graphical abstract

Antioxidant properties of ethanol extract of (milk thistle) seeds was investigated. We have also investigated the protein damage activated by oxidative Fenton reaction and its prevention by seed extract. Antioxidant potential of seed ethanol extract was measured using different methods, such as lipid peroxidation, 1,1-diphenyl-2-picrylhydrazyl (DPPH) and ferric reducing power assays. The extract significantly decreased DNA damage caused by hydroxyl radicals. Protein damage induced by hydroxyl radicals was also efficiently inhibited, which was confirmed by the presence of protein damage markers, such as protein carbonyl formation and by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The present study shows that milk thistle seeds have good DPPH free radical scavenging activity and can prevent lipid peroxidation. Therefore, can be used as potentially rich source of antioxidants and food preservatives. The results suggest that the seeds may have potential beneficial health effects providing opportunities to develop value-added products.

8-Oxoguanine DNA glycosylase 1 (OGG1) is a member of base excision repair, responsible for the repair of 8-oxoG base damage induced by reactive oxygen species. As oxidative DNA damage contributes to prostate carcinogenesis, investigating the interaction of OGG1 with prostate-specific proteins, which function in DNA damage and repair mechanisms in prostate cells, is important to determine appropriate therapeutic targets and ultimately support the cancer treatment strategies. Therefore, in this study we investigated the protein-protein interaction of OGG1 with androgen receptor (AR), which is critical for prostate cell proliferation as well as NKX3.1, which is a tumor suppressor protein specific to prostate cells. In addition, S326C, a polymorphic variant of OGG1 formed by a single amino acid change, has been reported in literature to cause a deficiency in repair activity leading OGG1 to be a predisposition factor for prostate cancer. In our immunoprecipitation results, OGG1 was detected to physically interact with NKX3.1 and AR upon increased oxidative DNA damage by menadione treatment. Further, immunofluorescence microscopy results showed that OGG1 localizes in the nuclear speckles at basal and induced level of DNA damage. Although NKX3.1 co-localize with OGG1 in the nucleus, localization of OGG1 was not observed in nuclear speckles in the presence of NKX3.1 possibly due to reduced oxidative DNA damage in NKX3.1 expressing cells. However, reduced physical association of OGG1-S326C variant form in comparison to wild type and further no co-localization of variant form with NKX3.1 was detected supporting the idea that OGG1-S326C variant form contributes to the prostate carcinogenesis.

Boron nitride nanotubes (BNNTs) represent an extremely interesting class of nanomaterials, and recent findings have suggested a number of applications in the biomedical field. Anyhow, extensive biocompatibility investigations are mandatory before any further advancement toward preclinical testing. Here, we report on the effects of multiwalled BNNTs in freshwater planarians, one of the best-characterized in vivo models for developmental biology and regeneration research. Obtained results indicate that BNNTs are biocompatible in the investigated model, since they do not induce oxidative DNA damage and apoptosis, and do not show adverse effects on planarian stem cell biology and on de novo tissue regeneration. In summary, collected findings represent another important step toward BNNT realistic applications in nanomedicine.

The protective effect of isoflavones on skin damage from ultraviolet (UV) radiation and their bioavailability were investigated in ovariectomized hairless mice fed diets composed of fermented soymilk containing aglycone forms of isoflavones or control soymilk containing glucose-conjugated forms of isoflavones. The erythema intensity of dorsal skin was significantly higher in ovariectomized mice than in sham-operated mice (p < 0.05). The erythema intensity and epidermal thickness of dorsal skin were significantly lower in the fermented soymilk diet group than in the control diet group (each p < 0.05). Levels of cyclobutane pyrimidine dimers in dorsal skin were significantly lower in the fermented soymilk diet group than in the control group (p < 0.05). Serum and dorsal skin isoflavone concentrations were significantly higher in the fermented soymilk diet group than in the soymilk diet group (p < 0.05). These results indicate that oral administration of a fermented soymilk diet increases isoflavone concentrations in the blood and skin, effectively scavenging the reactive oxygen species generated by UV irradiation and exerting an estrogen-like activity, with a consequent protective effect on skin photodamage in hairless mice.

The risk for cardiovascular diseases increases with age. Various markers for vascular aging have been suggested. However, these markers are not a direct measure of aging in vessels. Telomere length quantification can directly measure vascular aging—the current study aimed to investigate aging in aneurysm tissue by quantifying telomere length. Non‐diseased control vessels and ruptured and unruptured intracranial aneurysm vessels were resected during surgery. Telomere length quantification revealed a shorter telomere length in intracranial aneurysm tissue than in the non‐diseased control vessel. The difference in telomere length between non‐diseased control vessels and intracranial aneurysm tissue remained significant after normalizing for age. Moreover, the intracranial aneurysm tissue showed a lower expression of the aging marker Lamin B1 and a higher expression of the senescence marker P21. Additionally, intracranial aneurysm tissue presented higher activation of mTOR and NF‐κB pathways, which are known to contribute to inflammation and aging. Oxidative stress‐induced DNA damage appeared higher in intracranial aneurysm tissue than in non‐diseased control vessels. Our human data clearly showed increased molecular aging, elevated oxidative stress, and the activation of aging and inflammation‐associated pathways NF‐κB and mTOR in intracranial aneurysm tissue compared to non‐diseased control vessels. This study provides the first direct evidence of accelerated molecular aging in human intracranial aneurysm tissue, marked by telomere shortening, oxidative DNA damage, and activation of mTOR and NF‐κB pathways. These findings reveal critical aging‐related mechanisms potentially driving aneurysm formation and rupture.

Due to its health benefits, resveratrol (RE) is one of the most researched natural polyphenols. Resveratrol’s health benefits were first highlighted in the early 1990s in the French paradox study, which opened extensive research activity into this compound. Ever since, several pharmacological activities including antioxidant, anti-aging, anti-inflammatory, anti-cancerous, anti-diabetic, cardioprotective, and neuroprotective properties, were attributed to RE. However, results from the available human clinical trials were controversial concerning the protective effects of RE against diseases and their sequelae. The reason for these conflicting findings is varied but differences in the characteristics of the enrolled patients, RE doses used, and duration of RE supplementation were proposed, at least in part, as possible causes. In particular, the optimal RE dosage capable of maximizing its health benefits without raising toxicity issues remains an area of extensive research. In this context, while there is a consistent body of literature on the protective effects of RE against diseases, there are relatively few reports investigating its possible toxicity. Indeed, toxicity and adverse effects were reported following consumption of RE; therefore, extensive future studies on the long-term effects, as well as the in vivo adverse effects, of RE supplementation in humans are needed. Furthermore, data on the interactions of RE when combined with other therapies are still lacking, as well as results related to its absorption and bioavailability in the human body. In this review, we collect and summarize the available literature about RE toxicity and side effects. In this process, we analyze in vitro and in vivo studies that have addressed this stilbenoid. These studies suggest that RE still has an unexplored side. Finally, we discuss the new delivery methods that are being employed to overcome the low bioavailability of RE.

One of the major causes of defective sperm function is oxidative stress, which not only disrupts the integrity of sperm DNA but also limits the fertilizing potential of these cells as a result of collateral damage to proteins and lipids in the sperm plasma membrane. The origins of such oxidative stress appear to involve the sperm mitochondria, which have a tendency to generate high leve｜s of superoxide anion as a prelude to entering the intrinsic apoptotic cascade. Unfortunately, these cells have very little capacity to respond to such an attack because they only possess the first enzyme in the base excision repair （BER） pathway, 8-oxoguanine glycosylase 1 （OGG1）. The latter successfully creates an abasic site, but the spermatozoa cannot process the oxidative lesion further because they lack the downstream proteins （APE1, XRCC1） needed to complete the repair process. It is the responsibility of the oocyte to continue the BER pathway prior to initiation of S-phase of the first mitotic division. If a mistake is made by the oocyte at this stage of development, a mutation will be created that will be represented in every cell in the body. Such mechanisms may explain the increase in childhood cancers and other diseases observed in the offspring of males who have suffered oxidative stress in their germ line as a consequence of age, environmental or lifestyle factors. The high prevalence of oxidative DNA damage in the spermatozoa of male infertility patients may have implications for the health of children conceived in vitro and serves as a driver for current research into the origins of free radical generation in the germ line.