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Biochemical Indices of Fatigue for Anti-fatigue Strategies and Products
Published in Gerald Matthews, Paula A. Desmond, Catherine Neubauer, P.A. Hancock, The Handbook of Operator Fatigue, 2017
Yasuyoshi Watanabe, Hirohiko Kuratsune, Osami Kajimoto
As has previously been mentioned, metabolic processes may produce damaging oxidative molecules such as free radicals. 8-Oxo-deoxy-guanosine (8-OH-dG) (Asami et al., 1998; Shigenaga, Gimeno & Ames, 1989) and 8-isoprostane (Roberts & Morrow, 1994) in the tissues and urine are good biomarkers of moderate to severe exercise fatigue, due to DNA damage and lipid peroxidation, respectively. Lipid peroxidation refers to chemical changes in lipids such as fatty acids, which may lead to oxidative cell damage. We utilized both 8-OH-dG and 8-isoprostane for the development of an anti-fatigue food or drink component. For example, imidazole dipeptides, carnosine and anserine showed great antifatigue effects if they were taken before exercise, through the mechanisms of reduction of oxidative stress and immunosuppressive cytokine production, which resulted in lowering performance loss and fatigue sensation (Tanaka, Shigihara et al., 2008, as shown in Figure 14.3. (Cytokines are proteins important for communication between cells that modulate the functioning of the immune system, among other functions). Ascorbic acid (Vitamin C) and vitamin E levels also decreased in the peripheral tissues, mostly in the liver and kidney, after the fatigue load in animals, but their concentrations in the plasma and brain were constant, probably due to a compensatory process associated with the peripheral tissues.
Preclinical Characterization of Engineered Nanoparticles Intended for Cancer Therapeutics
Published in Mansoor M. Amiji, Nanotechnology for Cancer Therapy, 2006
Anil K. Patri, Marina A. Dobrovolskaia, Stephan T. Stern, Scott E. McNeil
Biomarkers of nanoparticle-induced oxidative stress measured in our laboratory include ROS, lipid peroxidation products, and GSH/GSSG ratio. The fluorescent dichlorodihydroflourescein (DCFH) assay is used for measurement of ROS, such as hydrogen peroxide.106 DCFH-DA is a ROS probe that undergoes intracellular deacetylation, followed by ROS-mediated oxidation to a fluorescent species, with excitation 485 nm and emission 530 nm. DCFH-DA can be used to measure ROS generation in the cytoplasm and cellular organelles, such as the mitochondria. The thiobarbituric acid reactive substances (TBARS) assay is used for measurement of lipid peroxidation products, such as lipid hydroperoxides and aldehydes. A molondialdehyde (MDA) standard curve is used for quantitation. MDA, a lipid peroxidation product, combines with thiobarbituric acid in a 1:2 ratio to form a fluorescent adduct, that is measured at 521 nm (excitation) and 552 nm (emission). TBARS are expressed as MDA equivalents.107 The dithionitrobenzene (DTNB) assay is used for evaluation of glutathione homeostasis. In the DTNB assay, reduced GSH interacts with 5,5′ -dithiobis(2-nitrobenzoic acid) (DTNB) to form the colored product 2-nitro-5-thiobenzoic acid, which is measured at 415 nm, and GSSG. GSSG is then reduced by glutathione reductase to form reduced GSH, which is again measured by the preceding method. Pretreatment with thiol-masking reagent, 1-methyl-4-vinyl-pyridinium trifluoromethane sulfonate, prevents GSH measurement, resulting in measurement of GSSG alone.108
Lead Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Rokeya Pervin, Md. Akil Hossain, Dipti Debnath, Mohiuddin Ahmed Bhuiyan
Lead toxicity is usually occurred by generating an increased amount of reactive oxygen species (ROS) and by interfering with an antioxidant generation [13]. Lead is not a redox-active element and it cannot directly play a role in those reactions which initiate the ROS formation. It was found that the generation of ROS in erythrocytes is increased by the interaction of lead with oxyhemoglobin [14]. The most significant contribution of lead in the initiation and expansion of oxidative stress is arisen by its interference with the enzymes and other cellular components/mechanisms of the defensive system which are responsible for preventing oxidative damage [15]. Glutathione (GSH), a tri-peptide of cysteine, histidine, and glutamate, is one of the most significant elements that protects cell components from ROS damage [2]. In healthy cells and tissues, 90% of GSH exists in reduced form and 10% in oxidized form, and it usually functions as an antioxidant defense mechanism. GSH after being converted (oxidized) to glutathione disulfide is reduced back to GSH by glutathione reductase [16]. Lead inactivates glutathione by binding to GSH’s sulphydryl group, which inhibits sulphydryl-dependent enzymes (e.g., glutathione reductase, superoxide dismutase, catalase, etc.) and causes GSH replenishment to become inefficient. Inhibition of these enzymes leads to the production of reactive oxygen species with resultant oxidative stress. The increase in oxidative stress leads to the damage of the cell membrane because of lipid peroxidation. Lead obstructs the activities of 5-aminolevulinic acid dehydratase and directs to hemoglobin oxidation, which together with the lipid peroxidation can cause hemolysis [17].
D-ribose-L-cysteine modulates paradoxical sleep deprivation-induced neurological impairments: anxiolytic and antioxidative study in rat model
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Taiwo Abayomi, Olorunfemi Tokunbo, Oluwatobiloba Oroyemi, Olawale Abayomi, Opeyemi Osuntokun, Benedict Falana, Temidayo Adeniyi
Sleep has been confirmed to limit metabolic requirements whereas sleep deprivation, on the other hand, enhances metabolic rate and in turn increases oxidative stress. Previous research has shown that sleep deprivation elicits psychotic episodes by induction of increased oxidative stress levels [35], triggered by increased metabolic activities. Lipid peroxidation is a known degenerative process of oxidation that leads to destruction of cell membranes, lipoproteins, and other lipid-containing structures [36]. Lipid peroxidation has been linked to a variety of neuropsychiatric disorders, including depression, schizophrenia, bipolar mood disorders, attention deficit hyperactivity disorder, and Alzheimer’s disease [37,38]. Previous studies have shown that increased serum lipid by-products, MDA and Lipid hydroperoxide (LOOH), are linked with patients with anxiety disorders [39,40]. This conforms to the findings in our present study, with increased serum MDA level observed in PSD which elicits lipid peroxidation and eventually elevated anxiety levels as seen in Figure 2. Whilst high anxiety levels have been established to significantly increase oxidative stress [41], it has also been shown that oxidative stress could trigger anxiety-related behavior [42]. However, D-Ribose-L-cysteine supplementation in this study revealed decreased serum lipid peroxidation evidenced by reduced MDA levels. This could be associated with its ability to prevent anxiogenic-like effects of sleep deprivation and its role as a bioactive source of antioxidants, therefore, reducing oxidative stress elicited by PSD.
Flavonoids fractions of Adansonia digitata L. fruits protects adult Wistar rats from mercury chloride-induced hepatorenal toxicity: histopathological and biochemical studies
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Wusa Makena, Yomi Samson Aribiyun, Aisha Aminu, Barka Ishaku, Ayuba Yohana, Ekwere Eke Inemesit
Heavy metals pollute the environment and are toxic to living organisms, and in their various forms, they exhibit distinct biological behavior, pharmacokinetics, and clinical manifestations [1–3]. It is commonly found in the environment and is linked to severe health issues in mammals, and exposure to mercury chloride (HgCl2) is via products like batteries, pesticides, and paints [1,4,5]. Mercury poisoning affects the nervous system, liver, kidney, and digestive system [6]. It is primarily metabolized in the liver before accumulating in the kidneys. As a result, the liver and kidneys are the organs most affected [7]. Mercury chloride poisoning has previously been shown to occur via several routes, including inhalation, ingestion, and skin absorption [8]. Mercury chloride also degrades antioxidants and reduces free radical scavenging systems like superoxide dismutase (SOD), Catalase (CAT) and reduced glutathione (GSH) [9–11]. The occurrence of lipid peroxidation is among the critical pathological factors in the sequence of events that leads to the onset of degenerative diseases due to disruptions in redox and calcium homeostasis [12,13].
Insights into the potential mechanism underlying liver dysfunction in male albino rat exposed to gasoline fumes
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Folarin Owagboriaye, Sulaimon Aina, Rasheed Oladunjoye, Titilola Salisu, Adedamola Adenekan, Gabriel Dedeke
Lipid peroxidation was evaluated by measuring its end product, malondialdehyde (MDA), as thiobarbituric acid reactive substance [TBARS) in TBARS assay described by [22, 23]. Concentration of reduced glutathione (GSH] was determined by employing an established protocol (Hassan and Barakat, 24), which is based on the formation of 2-nitro-S-mercaptobenzoic per mole of glutathione through the reduction of 5,5-dithiobis-2 nitrobenzoic acid (DTNB) by SH groups of glutathione. The concentration of GSH was quantified spectrophotometrically at 412 nm using the extinction coefficient of 13.7 mM−1 cm−1. Activity of catalase [CAT) was measured spectrophotometrically according to [25]. Superoxide dismutase [SOD] activity was according to [26], while glutathione peroxidase [GPx] activity was determined according to [27].