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Luis J. Flores

Researcher at University of Texas Health Science Center at San Antonio

Publications -  9
Citations -  2871

Luis J. Flores is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Melatonin & Pineal gland. The author has an hindex of 9, co-authored 9 publications receiving 2632 citations. Previous affiliations of Luis J. Flores include University of Texas at San Antonio.

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One molecule, many derivatives: a never-ending interaction of melatonin with reactive oxygen and nitrogen species?

TL;DR: This review focuses on melatonin metabolism which includes the synthetic rate‐limiting enzymes, synthetic sites, potential regulatory mechanisms, bioavailability in humans, mechanisms of breakdown and functions of its metabolites.
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Melatonin and its metabolites: new findings regarding their production and their radical scavenging actions.

TL;DR: The review makes the point that melatonin's actions are uncommonly widespread in organs due to the fact that it works via membrane receptors, nuclear receptors/binding sites and receptor-independent mechanisms, i.e., the direct scavenging of free radicals.
Journal Article

Medical implications of melatonin: receptor-mediated and receptor-independent actions.

TL;DR: Among the actions of melatonin that are likely receptor independent and that are reviewed herein include its ability to neutralize free radicals which leads to a reduction in cataract formation, reducing oxidative stress due to exposure to hyperbaric hyperoxia, ameliorating hyperthyroidism and abating the toxicity of sepsis and septic shock.
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Melatonin and pregnancy in the human.

TL;DR: Melatonin is a neuroendocrine hormone secreted nightly by pineal gland and regulates biological rhythms and it appears to be essential for successful pregnancy.
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The potential of melatonin in reducing morbidity-mortality after craniocerebral trauma.

TL;DR: Melatonin crosses the blood–brain barrier and reduces contusion volume and stabilizes cellular membranes preventing vasospasm and apoptosis of endothelial cells that occurs as a result of CCT.