Effect of Epigallocatechin-3- Gallate and Quercetin on the Production of Reactive Oxygen and Nitrogen Species in Liver of Rats Exposed to Round-the-Clock Light and Kept on Carbohydratelipid Diet

Abstract

The purpose of this study is to investigate the effects of bioflavonoids, epigallocatechin-3-gallate (EGCG) and quercetin, on the production of reactive oxygen and nitrogen species in the liver of rats under round-the-clock light exposure with an intensity of 1500 lux for 30 days while being kept on carbohydrate-lipid diet (20% fructose solution and appropriate food) for 60 days. In the liver tissues, the rate of the superoxide anion production by NADPH-dependent electron transport chains (microsomal monooxygenases and constitutive uncoupled NO synthases) increased by 1.93 times, by the mitochondrial respiratory chain by 1.89 times, and it was doubled by leukocyte NADPH-oxidase. The total activity of NO synthase was increased by 2.35 times, the activity of its inducible isoform increased by 2.57 times, and the concentration of alkali and alkaline earth metals peroxynitrites elevated by 1.68 times. Administration of bioflavonoids-epigallocatechin-3-gallate and quercetinsignificantly restrained the rate of superoxide anion production in the liver tissues by microsomal monooxygenases and NO synthase by 39.1 and 40.1%, by the mitochondrial respiratory chain by 37.2 and 34.4%, by leukocyte NADPH-oxidase by 35.0 and 32.1%, respectively. Epigallocatechin-3-gallate and quercetin inhibited the total activity of NO-synthase by 46.7 and 36.2%, the activity of its inducible isoform by 49.6 and 39,0%, increased the activity of the constitutive isoenzyme NO-synthase by 2.9 times and its coupling index by 4.5 and 4.7 times. Additionally, administration of these bioflavonoids lowered the concentration of peroxynitrites of alkali and alkaline earth metals by 30.5 and 34.3% compared to the respective values obtained in the group of rats, which did not receive the bioflavonoids, but were exposed to light and carbohydrate-lipid-rich diet. We suggest that epigallocatechin3-gallate and quercetin in the above experimental conditions are effective means to restrain the formation of reactive oxygen and nitrogen species in the liver tissue.

Dietary Supplementation with Resveratrol Attenuates Serum Melatonin Level, Pro-Inflammatory Response and Metabolic Disorder in Rats Fed High-Fructose High-Lipid Diet under Round-the-Clock Lighting

“…The rats were kept on a HFHLD for 2 months: the animals received a 20% aqueous solution of fructose for drinking and ahigh-lipid diet, whose components and content are given in Table 1 . Fromthe 30th day of the experiment, the rats were exposed to RCL with an intensity of 1500 lx over the next 30 days, as previously reported [ 23 ].…”

Desmodium styracifolium: Botanical and ethnopharmacological insights, phytochemical investigations, and prospects in pharmacology and pharmacotherapy

“…Moreover, flavonoids possess the ability to modulate the activation of the SIRT1 cascade, which in turn, blocks the activation of NF-κB [ 87 ], and modulate NF-κB activation through Toll-like receptor (TLR) type 4 [ 81 ]. The inhibitory effect of flavonoids on oxidative and nitrosative stress in various organs can also be attributed to their ability to inhibit the Janus kinase (JAK) transcriptional cascade – signal transducers and activators of transcription (STAT) [ 88 , 89 ], as well as their ability to induce the Nrf2/antioxidant-responsive element (ARE) signalling pathway [ [90] , [91] , [92] ]. Additionally, flavonoids are able to activate the antioxidant response of the cell through peroxisome proliferator-activated receptors (PPAR) γ [ 93 ].…”

Modulation of redox-sensitive transcription factors with polyphenols as pathogenetically grounded approach in therapy of systemic inflammatory response

“…NFκB-dependent formation of the LGSIP is reported in cases of the disruption of light/dark cycle [ 80 ], high-calorie diet [ 81 ], exposure to ionizing radiation [ 82 ] and toxic factors [ 21 ]. There have been identified a number of genetic disorders of the IKK-IKB-NFκB system that can cause autoimmune and inflammatory diseases, malignant tumours, and critical changes in the morphogenesis and regeneration [ 83 ].…”