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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Vitamin B2 or riboflavin is an essential vitamin of group B. It is a water-soluble, yellow-orange organic compound and is heat stable. Riboflavin is the central component of the coenzymes: flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), and acts as a co-factor in numerous enzymatic reactions. It is therefore important for energy production, enzyme function, and normal protein, fatty acid and amino acid synthesis (3, 9, 33, 37–38). It mediates the transfer of electrons in biological oxidation-reduction reactions. It is also involved in the metabolism of folate, vitamin B12, vitamin B6, and other vitamins. It also helps to maintain the integrity of mucous membranes, skin, the eyes and nervous system (38). The role of riboflavin has also been credited in the prevention of a wide array of health diseases like migraine, anemia, cancer, hyperglycemia, hypertension, diabetes mellitus, and oxidative stress, directly or indirectly (38). A deficiency of riboflavin named ariboflavinosis is manifested in swollen tongue, skin eruption, and eye irritation (3, 33, 37–38). Riboflavin deficiency has profound effects on iron absorption, metabolism of tryptophan, mitochondrial dysfunction, the gastrointestinal tract, brain dysfunction, and metabolism of other vitamins (38). Although riboflavin is involved in all areas of metabolism, and deficiency is widespread on a global scale, deficiency is not fatal (33). Riboflavin deficiency is usually associated with other vitamin B complex deficiencies; isolated riboflavin deficiency is rare (3, 33).
Basal Redox Status Influences the Adaptive Redox Response to Regular Exercise
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Ethan L. Ostrom, Tinna Traustadóttir
Oxidative eustress initiates adaptive processes in response to exercise that stem from multiple enzymatic sources in the cell. These processes initiate cell signaling cascades through protein thiol oxidation/reduction reactions that improve cellular metabolism and increase redox stress response capacity. These increases in mitochondrial biogenesis and the antioxidant defense system are governed partly by the inducible redox stress response transcription factor, Nrf2. Increases in Nrf2 activation and downstream target genes occur in response to acute exercise through a combination of ROS sources. The chronic increases in basal or resting levels of mitochondrial ROS from sedentary behavior, overfeeding, and age-related mitochondrial dysfunction increase basal levels of Nrf2, which likely impairs the Nrf2 signaling system from responding further to an added transient oxidative eustress like exercise. This is exacerbated by the feed-forward redox signaling mechanisms elicited by the initial adaptive response to increasing basal ROS production, simultaneously protecting the cell from its own dysfunctional redox circuitry and making it harder for transient oxidative eustress signals like exercise to be effective.
Bacteria are harmless
Published in Dinesh Kumar Jain, Homeopathy, 2022
The most important prerequisite for the conversion of clostridial contamination of a wound to a progressive infection is an environment with low oxidation reduction potential, which permits spore germination and anaerobic growth. Local oxidation reduction potential can be reduced by failure of the blood supply to a contaminated area or by multiplication of other bacteria in the wound. Once multiplication and toxin production are established rapid invasion and destruction of healthy tissue follows.
An approach to assessing the contribution of the high LET effect in strategies for Auger endoradiotherapy
Published in International Journal of Radiation Biology, 2023
Pavel Lobachevsky, Colin Skene, Laura Munforte, Andrea Smith, Jonathan White, Roger F. Martin
In order to understand the impact of RBE on the extent of radioprotection by methylproamine and analogs, it is important to consider the proposed mechanism of radioprotection, starting from an ionization event on DNA, such as extraction of an electron to form, for example, a guanine radical cation. This is a transient lesion that is a precursor to permanent DNA damage. Next, consider a minor groove binding radioprotector nearby to this lesion. The transient DNA lesion species is an oxidizing agent, whereas the ligand is a reductant. An oxidation-reduction reaction takes place, mediated by charge transfer within the DNA molecule. It is known from pulse radiolysis experiments (Martin and Anderson 1998) that the range of this charge transfer is of the order of 30 base pairs. The overall outcome is that the initial lesion is repaired and the ligand is oxidized. The mechanism is analogous to the so-called sacrificial anode, whereby a Zn electrode is attached, with an electrical connection, to steel. The Zn is preferentially oxidized, and the Fe is protected.
The genotoxic effects of mixture of aluminum, arsenic, cadmium, cobalt, and chromium on the gill tissue of adult zebrafish (Danio rerio, Hamilton 1822)
Published in Drug and Chemical Toxicology, 2022
Fulya Dilek Gökalp, Oğuzhan Doğanlar, Zeynep Banu Doğanlar, Utku Güner
Cobalt (Co+2) and Chromium (Cr+2), two commonly found metals, are considered to be harmful to human health (Valko et al. 2005). Moreover, they can cause acute toxicity and cancer in the long-term (Fu and Boffetta 1995). Following exposure, it has been shown that Cr+2 and Co+2 changed 696 and 461 types of gene expressions, respectively, in zebrafish (Ventura-Lima et al. 2009, Baer et al. 2014). These are expressions for the adaptive response genes which control the acute phase response, cell cycle regulation, apoptosis, and metabolic suppression (Baer et al. 2014). It has been found that there is a concentration-response relationship between fish death and concentrations of Co+2 and Cr+2. They are also purported to suppress the regulation of the biological processes associated with the oxidative stress response, including oxidation–reduction (Hussainzada et al. 2014). It was also indicated that Cr(IV) induced oxidative stress in Anguilla anguilla (Ahmad et al. 2006), and that the genotoxicity was due to free radicals which led to the crosslinking of DNA proteins (Lushchak et al.2008) and further induced micronucleus and tail DNA (Comet assay) after both 48-h and 96-h Cr(IV) exposures (Ahmed et al. 2013).
The role of radiation induced oxidative stress as a regulator of radio-adaptive responses
Published in International Journal of Radiation Biology, 2020
Mohsen Sisakht, Maryam Darabian, Amir Mahmoodzadeh, Ali Bazi, Sayed Mohammad Shafiee, Pooneh Mokarram, Zahra Khoshdel
Mitochondria are also affected by ionizing radiation-induced oxidative stress, and play a critical role in response to this condition. In a normal state, mitochondria are one of the cites for intracellular ROS production, mainly due to electron leakage from electro transport chain. When cells are exposed to the ionizing radiation, mitochondrial functions could be directly disrupted. Possible consequences are imbalanced oxidation-reduction interactions, mitochondrial dysfunction and aberrant expression of crucial proteins in cellular and mitochondrial functions. Overproduction of free radicals, in the cells exposed to ionizing radiation, could also lead to mutations and changes in the copy number of mitochondrial DNA (mtDNA). Insulted cells also show damaged mitochondrial DNA polymerase and aberrant inexpression of components of mitochondrial electron transport chain.