Estradiol Modulates Membrane-Linked ATPases, Antioxidant Enzymes, Membrane Fluidity, Lipid Peroxidation, and Lipofuscin in Aged Rat Liver

Abstract

Free radical production and oxidative stress are known to increase in liver during aging, and may contribute to the oxidative damage. These changes increase during menopausal condition in females when the level of estradiol is decreased. The objective of this study was to observe the changes in activities of membrane linked ATPases (Na+K+ ATPase, Ca2+ ATPase), antioxidant enzymes (superoxide dismutase, glutathione-S-transferase), lipid peroxidation levels, lipofuscin content and membrane fluidity occurring in livers of female rats of 3, 12 and 24 months age groups, and to see whether these changes are restored to 3 months control levels rats after exogenous administration of 17-β-estradiol (E2). The aged rats (12 and 24 months) were given subcutaneous injection of E2 (0.1 μg/g body weight) daily for one month. The results obtained in the present work revealed that normal aging was associated with significant decrease in the activities of membrane linked ATPases, antioxidant enzymes, membrane fluidity and an increase in lipid peroxidation and lipofuscin content in livers of aging female rats. The present study showed that E2 treatment reversed the changes to normal levels. E2 treatment may be beneficial in preventing some of the age related changes in the liver by increasing antioxidant defenses.

A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and sickness behavior

“…Elevated MDA promotes phospholipids rigidity, altering membrane fluidity, permeability and transport mechanisms [136]. Importantly, elevated MDA decreases mitochondrial membrane fluidity [137]. A decrease in melatonin, found in some ME/CFS studies, would contribute to increased mitochondrial membrane rigidity [138], as well as reduced natural killer cell activity in ME/CFS [119].…”

<p>Gold nanoparticle uptake is enhanced by estradiol in MCF-7 breast cancer cells</p>

“…This mechanism can be used by different types of cells to uptake and internalize 20–45 nm AuNPs52,53 by receptor-mediated endocytosis. In contrast, because E 2 interacts with the membrane surface, it has been shown to significantly modulate membrane fluidity in different cell models, as measured by fluorescence polarization using the fluorescent dye DPH (1,6-diphenyl-hexa-1,3,5-triene) 54,55. However, the effects of incubating cells with E 2 together with AuNPs have remained largely uninvestigated.…”

Edaravone Mitigates Hexavalent Chromium-Induced Oxidative Stress and Depletion of Antioxidant Enzymes while Estrogen Restores Antioxidant Enzymes in the Rat Ovary in F1 Offspring1

“…E 2 depletion leads to apoptosis and DNA damage, as well as elevated oxidative stress in the lymphocytes of rats, which is reversed by supplementing E 2 [63]. E 2 supplementation reversed the age-related depletion of AOX enzymes and increase in free radicals in rat liver [64]. Therefore, the current study suggests that the decrease in steroidogenesis due to increased follicular atresia may predispose the ovary to decreased AOX enzyme gene transcription and activity, resulting in oxidative stress.…”