Melatonin is a potential therapeutic molecule for oxidative stress induced red blood cell (RBC) injury : A review

Banerjee, Adrita; Chattopadhyay, Aindrila; Pal, Palash Kumar; Bandyopadhyay, Debasish

doi:10.32794/mr11250045

Cited by 5 publications

(2 citation statements)

References 198 publications

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“…Melatonin is an important member of the antioxidant system [ 95 ]. It is a potent direct free radical scavenger and also acts as an indirect antioxidant by enhancing the activities of antioxidant enzymes including mitochondrial SODs, catalase and glutathione reductase [ 96 , 97 ]. Importantly, it has the potential of reducing mitochondrial ROS generation by upregulating the activity of UCP1 (uncoupling protein 1) in brown adipose tissue [ 98 , 99 ] and UCP 3 in cardiomyocytes [ 100 ].…”

Section: Mitochondria and Melatoninmentioning

confidence: 99%

Targeting Host Defense System and Rescuing Compromised Mitochondria to Increase Tolerance against Pathogens by Melatonin May Impact Outcome of Deadly Virus Infection Pertinent to COVID-19

Tan¹,

Hardeland

2020

Molecules

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Fighting infectious diseases, particularly viral infections, is a demanding task for human health. Targeting the pathogens or targeting the host are different strategies, but with an identical purpose, i.e., to curb the pathogen’s spreading and cure the illness. It appears that targeting a host to increase tolerance against pathogens can be of substantial advantage and is a strategy used in evolution. Practically, it has a broader protective spectrum than that of only targeting the specific pathogens, which differ in terms of susceptibility. Methods for host targeting applied in one pandemic can even be effective for upcoming pandemics with different pathogens. This is even more urgent if we consider the possible concomitance of two respiratory diseases with potential multi-organ afflictions such as Coronavirus disease 2019 (COVID-19) and seasonal flu. Melatonin is a molecule that can enhance the host’s tolerance against pathogen invasions. Due to its antioxidant, anti-inflammatory, and immunoregulatory activities, melatonin has the capacity to reduce the severity and mortality of deadly virus infections including COVID-19. Melatonin is synthesized and functions in mitochondria, which play a critical role in viral infections. Not surprisingly, melatonin synthesis can become a target of viral strategies that manipulate the mitochondrial status. For example, a viral infection can switch energy metabolism from respiration to widely anaerobic glycolysis even if plenty of oxygen is available (the Warburg effect) when the host cell cannot generate acetyl-coenzyme A, a metabolite required for melatonin biosynthesis. Under some conditions, including aging, gender, predisposed health conditions, already compromised mitochondria, when exposed to further viral challenges, lose their capacity for producing sufficient amounts of melatonin. This leads to a reduced support of mitochondrial functions and makes these individuals more vulnerable to infectious diseases. Thus, the maintenance of mitochondrial function by melatonin supplementation can be expected to generate beneficial effects on the outcome of viral infectious diseases, particularly COVID-19.

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Section: Mitochondria and Melatoninmentioning

confidence: 99%

Targeting Host Defense System and Rescuing Compromised Mitochondria to Increase Tolerance against Pathogens by Melatonin May Impact Outcome of Deadly Virus Infection Pertinent to COVID-19

Tan¹,

Hardeland

2020

Molecules

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“…However, excessive ROS levels under hyperglycemia result in oxidative stress, leading to cell and tissue damage. Indeed, melatonin is a potent direct free radical scavenger and also acts as an indirect antioxidant by enhancing the activities of antioxidant enzymes including mitochondrial superoxide dismutases (SODs), catalase, and glutathione reductase ( 38 ). Thus, substantially high melatonin is required for stabilizing the mitochondrial functions, especially in the antioxidant system ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Melatonin Maintains Inner Blood–Retinal Barrier by Regulating Microglia via Inhibition of PI3K/Akt/Stat3/NF-κB Signaling Pathways in Experimental Diabetic Retinopathy

et al. 2022

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Microglial activation and melatonin protection have been reported in diabetic retinopathy (DR). Whether melatonin could regulate microglia to protect the inner blood–retinal barrier (iBRB) remains unknown. In this study, the role of microglia in iBRB breakdown and the mechanisms of melatonin’s regulation on microglia were explored. In diabetic rat retinas, activated microglia proliferated and migrated from the inner retina to the outer retina, accompanied by the obvious morphological changes. Meanwhile, significant leakage of albumin was evidenced at the site of close interaction between activated microglia and the damaged pericytes and endothelial cells. In vitro, inflammation-related cytokines, such as tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, and arginase-1 (Arg-1), were increased significantly in CoCl2-treated BV2 cells. The supernatant derived from CoCl2-treated BV2 cells significantly decreased the cell viability and disrupted the junctional proteins in both pericytes and endothelial cells, resulting in severe leakage. Melatonin suppressed the microglial overactivation, i.e., decreasing the cell number and promoting its anti-inflammatory properties in diabetic rat retinas. Moreover, the leakage of iBRB was alleviated and the pericyte coverage was restored after melatonin treatment. In vitro, when treated with melatonin in CoCl2-treated BV2 cells, the inflammatory factors were decreased, while the anti-inflammatory factors were increased, further reducing the pericyte loss and increasing the tight junctions. Melatonin deactivated microglia via inhibition of PI3K/Akt/Stat3/NF-κB signaling pathways, thus maintaining the integrity of iBRB. The present data support a causal role for activated microglia in iBRB breakdown and highlight the therapeutic potential of melatonin in the treatment of DR by regulating microglia.

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Erythrocyte membrane integrity and protein activity in high-fat diet fed male Wistar rats

Ogbara

Adele²,

Ige³

et al. 2022

Nutrire

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High fat diet (HFD) has been reported to induce systemic in ammation and oxidative stress that may affect the structural integrity of erythrocytes and alter their ability to undergo deformation. This study was therefore designed to investigate the effect of HFD feeding on erythrocyte membrane integrity and protein activity in male Wistar rats. MethodsTen animals (100-120g) were grouped equally and exposed to either standard diet or HFD (25%-fat) for 42days. Thereafter, retro-orbital sinus blood was collected under anesthesia (thiopental) and aliquots were analyzed for erythrocyte sedimentation rate (ESR), osmotic fragility and mean corpuscular fragility.Erythrocyte ghost membranes were also isolated from blood sample aliquots and analyzed for total protein concentration, malondialdehyde (MDA), Na + K + -ATPase activity, Ca 2+ Mg 2+ -ATPase activity and intercellular adhesion molecule (ICAM)-4 level. ResultsOsmotic fragility and mean corpuscular fragility were signi cantly increased (P<0.05) in the HFD-fed group compared to control. ESR (mm/hr) (64.60±2.34 vs. 21.20±1.53), membrane MDA (µMol) (3.66±0.86 vs. 0.43±0.08) and ICAM-4 (ng/ml) (1.68±0.23 vs. 0.49±0.16) levels were also increased (P<0.05) in the group 2 (HFD) compared to group 1 (standard diet). Compared to standard diet group, erythrocyte membrane total protein concentration (10.46±0.96 vs 6.00±0.38 g/dl) and Na + K + ATPase activity (1.37±0.22 vs 0.22±0.03 x10 7 µmol pi/mg protein/hr) was reduced (P<0.05) in the HFD group while Ca 2+ Mg 2+ -ATPase exhibited a 27.9% increase in activity. ConclusionThis study suggests that high fat diet may compromise the structural and functional integrity of erythrocytes by activating systemic in ammation, erythrocyte membrane and protein oxidation as well dysregulated membrane ATPase activity required to maintain erythrocyte deformability in male Wistar rat.

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Melatonin is a potential therapeutic molecule for oxidative stress induced red blood cell (RBC) injury : A review

Cited by 5 publications

References 198 publications

Targeting Host Defense System and Rescuing Compromised Mitochondria to Increase Tolerance against Pathogens by Melatonin May Impact Outcome of Deadly Virus Infection Pertinent to COVID-19

Targeting Host Defense System and Rescuing Compromised Mitochondria to Increase Tolerance against Pathogens by Melatonin May Impact Outcome of Deadly Virus Infection Pertinent to COVID-19

Melatonin Maintains Inner Blood–Retinal Barrier by Regulating Microglia via Inhibition of PI3K/Akt/Stat3/NF-κB Signaling Pathways in Experimental Diabetic Retinopathy

Erythrocyte membrane integrity and protein activity in high-fat diet fed male Wistar rats

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