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Cold- and heat-related illness is greatly impacted by a variety of factors that can affect the swimming athlete. Both occur when there is a thermoregulatory mismatch between heat production from exercise and heat loss. Body heat loss in the swimmer primarily occurs through convection from the interface of the skin and water that is proportional to speed (heat transfer coefficient) and the temperature difference between the skin and water [110]. Other factors impacting heat loss include the design and thermal properties of garments, the environment (air temperature, humidity), athlete illness, and medications [111, 112].
Antioxidants have been shown to interact with and neutralize free radicals and defuse their effects, which include gene mutation, oxidative damage to chromosomes and proteins, lipid peroxidation of cellular membranes, and dysfunctional cell growth [5]. The brain consists of 20% of the total metabolic activity of the body and has a higher consumption of oxygen than other tissues [6, 7]. Thus, it is thought to be a possible site for oxidative stress (OS) damage, which may encourage the development of brain cancer. Genomic instability caused by OS-mediated damage to cellular macromolecules encourages the development of cancer. Reactive oxygen species (ROS)-sensitive cell signaling events are implicated in the proliferation, growth, differentiation, metabolism, inflammation, angiogenesis, and survival of cancer cells. A growing body of evidence have also revealed the role of ROS in promoting drug resistance in brain tumors [8]. The antioxidant capacity of the brain is significantly lower than other tissues [9]. Endogenous antioxidants involve heterogeneous groups that are water or lipid-soluble enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), etc., and some cellular metabolites like reduced glutathione (GSH) and thioredoxin [10]. Various studies have reported that antioxidant systems such as SOD and thioredoxin play a key role in protecting cells from ROS-induced damages [11,12,13].
GSH, γ-l-glutamyl-l-cysteinyl-glycine, is an antioxidant tripeptide that is mainly found in the cytosol of a cell. This low molecular weight thiol plays a vital role in sustaining the intracellular redox balance. GSH with GSH-regulated enzymes constitutes a redox defense system in the brain and exhibits neuroprotective effects. It has a great role in the modulation of enzyme activity, activation of DNA repair, and regulation of transcription factors and different metabolic processes [182, 183]. GSH also plays a key role in the detoxification and elimination of carcinogen and imparts a chemopreventive role [184]. Significant variability of GSH levels was seen in different types of cancers; however, accumulating evidence shows that the majority of brain tumor cases are associated with depletion of GSH levels in brain tumor tissue compared with healthy brain tissue [38, 46]. However, conflicting reports also noted that brain tumor patients showed a higher level of GSH [31]. In a previous report, Kudo and colleagues demonstrated that only meningiomas exhibit extremely high GSH levels, in contrast to other forms of brain tumors, such as GBM, gliomas, germinoma, multiple myeloma, and small-cell carcinoma [45]. Moreover, GSH levels also serve as a prognostic marker of the malignancy of brain cancer. High grade (III/IV) gliomas and astrocytomas exhibit significantly lower GSH levels compared with low grade (I/II) tumors [38, 185]. High levels of ROS production during tumor progression have been implicated in the reduction of GSH and GSH-associated enzymatic activities. Chemotherapeutic drug like 5-fluorouracil can reduce tumor growth by inducing apoptosis but can neither improve redox status nor GSH level in non-primary brain tumor bearing mice [186]. NAC, a GSH precursor has shown promise of inhibiting proliferation, growth, invasion, and migration of glioblastoma cells, as well as of inducing apoptosis by dowregulating neurogenic locus notch homolog protein 2 (Notch2) signaling pathways. The effect seems to be independent of GSH and ROS levels in glioblastoma cells [187]. This report may indicate that enhancement of GSH levels may not be a therapeutic approach in brain tumor treatment. Moreover, emerging evidence revealed the positive association between GSH and chemoresistance in different types of cancers including brain cancers [188, 189]. The chemoresistance in primary brain tumors may arise due to the interplay between multidrug resistance-associated protein-triggered efflux of the drug-GSH conjugate and GST/GSH-provoked drug detoxification [188]. Thus, GSH inhibition may reverse drug resistance to improve chemotherapeutic efficacy. A strategy like using buthionine sulfoximine to directly deplete GSH has been investigated to improve the chemotherapy efficacy in brain cancers; however, lack of selectivity for tumor cells and nonspecific organ toxicity restricts its clinical application [188, 190,191,192]. Thus, it would not be wrong to mention that GSH acts as a double-edged sword. On the one hand, it inhibits the initiation of cancer by metabolizing carcinogens. On the other hand, its detoxification action restricts the chemotherapeutic effect of drugs and supports the chemoresistance of cancer cells. Inclusion of GSH as a formulation component could aid the therapeutic efficacy of chemotherapeutic drugs. GSH functionalization of a formulation facilitates crossing the BBB mediated through the GSH transporter and may deliver the drug to the brain. GSH-PEG (polyethylene glycol)-ylated liposomal doxorubicin improves therapeutic efficacy by increasing doxorubicin concentration in the brain without altering BBB integrity [193, 194]. Transferrin-targeted GSH-sensitive hyaluronic acid-poly(lactic-co-glycolic acid) nanomicelle loaded with a heat shock protein 90 (Hsp90) inhibitor, AUY922 to enhance the therapeutic efficacy towards brain cancers. GSH conjugation allows fast release of AUY922 to the tumor site and cellular uptake through transferrin receptor [195]. 153554b96e
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