1,721,082 research outputs found
H2S: a "double face" molecule in health and disease.
No full textH2S is a colorless, poisonous, and flammable gas with the characteristic foul odor of rotten eggs. H2S is present in effluent from hydrothermal vents and sulfur springs, which have been proposed to act as "pores" in the Earth surface, providing a source of energy in the form of reducing equivalents and of iron-sulfur centers. Remarkably, H2S-producing machineries or H2S-utilization capacity remain within a great diversity of microorganisms. In particular, two classes of bacteria have been identified, that is, sulfate- and sulfur-reducing and sulfur-oxidizing bacteria, both contributing to the balance of the H2S level. The human body produces H2S and uses it as a signaling molecule in several physiological processes. However, many diseases, including neurological diseases, cardiovascular diseases, inflammation, and metabolic disorders, have been linked to abnormal endogenous H2S functions and metabolism. Remarkably, in recent years, the therapeutic administration of H2S(-donors) appears relevant in the treatment of some diseases. Here, H2S metabolism, as well as its physiological and pathological roles in humans is reviewed. Furthermore, the therapeutic use of H2S is discussed
Carbon monoxide: an unusual drug
No full textThe highly toxic gas carbon monoxide (CO) displays many physiological roles in several organs and tissues. Although many diseases, including cancer, hematological diseases, hypertension, heart failure, inflammation, sepsis, neurodegeneration, and sleep disorders, have been linked to abnormal endogenous CO metabolism and functions, CO administration has therapeutic potential in inflammation, sepsis, lung injury, cardiovascular diseases, transplantation, and cancer. Here, insights into the CO-based therapy, characterized by the induction or gene transfer of heme oxygenase-1 and either gas or CO-releasing molecule administration, are reviewed
Oncogenic disruption of promyelocytic leukemia nuclear bodies in APL cells results in defects in DNA double strand breaks sensing and repair
No full textNBN Gene Polymorphisms and Cancer Susceptibility: A Systemic Review. * di Masi A. and Antoccia A. are co-corresponding authors of this work.
No full textThe relationship between DNA repair failure and cancer is well established as in the case of rare, high penetrant genes in high cancer risk families. Beside this, in the last two decades, several studies have investigated a possible association between low penetrant polymorphic variants in genes devoted to DNA repair pathways and risk for developing cancer. This relationship would be also supported by the observation that DNA repair processes may be modulated by sequence variants in DNA repair genes, leading to susceptibility to environmental carcinogens. In this framework, the aim of this review is to provide the reader with the state of the art on the association between common genetic variants and cancer risk, limiting the attention to single nucleotide polymorphisms (SNPs) of the NBN gene and providing the various odd ratios (ORs). In this respect, the NBN protein, together with MRE11 and RAD50, is part of the MRN complex which is a central player in the very early steps of sensing and processing of DNA double-strand breaks (DSBs), in telomere maintenance, in cell cycle control, and in genomic integrity in general. So far, many papers were devoted to ascertain possible association between common synonymous and non-synonymous NBN gene polymorphisms and increased cancer risk. However, the results still remain inconsistent and inconclusive also in meta-analysis studies for the most investigated E185Q NBN miscoding variant
CO metabolism, sensing, and signaling. * di Masi A. and Gullotta F. contributed equally to this work.
No full textCO is a colorless and odorless gas produced by the incomplete combustion of hydrocarbons, both of natural and anthropogenic origin. Several microorganisms, including aerobic and anaerobic bacteria and anaerobic archaea, use exogenous CO as a source of carbon and energy for growth. On the other hand, eukaryotic organisms use endogenous CO, produced during heme degradation, as a neurotransmitter and as a signal molecule. CO sensors act as signal transducers by coupling a "regulatory" heme-binding domain to a "functional" signal transmitter. Although high CO concentrations inhibit generally heme-protein actions, low CO levels can influence several signaling pathways, including those regulated by soluble guanylate cyclase and/or mitogen-activated protein kinases. This review summarizes recent insights into CO metabolism, sensing, and signaling
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