Affordable Access

Access to the full text

Chlorella sorokiniana Dietary Supplementation Increases Antioxidant Capacities and Reduces ROS Release in Mitochondria of Hyperthyroid Rat Liver

Authors
  • Napolitano, Gaetana
  • Fasciolo, Gianluca1
  • Salbitani, Giovanna1
  • Venditti, Paola
  • 1 (G.S.)
Type
Published Article
Journal
Antioxidants
Publisher
MDPI AG
Publication Date
Sep 17, 2020
Volume
9
Issue
9
Identifiers
DOI: 10.3390/antiox9090883
PMID: 32957734
PMCID: PMC7555375
Source
PubMed Central
Keywords
License
Green

Abstract

The ability of aerobic organisms to cope with the attack of radicals and other reactive oxygen species improves by feeding on foods containing antioxidants. Microalgae contain many molecules showing in vitro antioxidant capacity, and their food consumption can protect cells from oxidative insults. We evaluated the capacity of dietary supplementation with 1% dried Chlorella sorokiniana strain 211/8k, an alga rich in glutathione, α-tocopherol, and carotenoids, to counteract an oxidative attack in vivo. We used the hyperthyroid rat as a model of oxidative stress, in which the increase in metabolic capacities is associated with an increase in the release of mitochondrial reactive oxygen species (ROS) and the susceptibility to oxidative insult. Chlorella sorokiniana supplementation prevents the increases in oxidative stress markers and basal oxygen consumption in hyperthyroid rat livers. It also mitigates the thyroid hormone-induced increase in maximal aerobic capacities, the mitochondrial ROS release, and the susceptibility to oxidative stress. Finally, alga influences the thyroid hormone-induced changes in the factors involved in mitochondrial biogenesis peroxisomal proliferator-activated receptor-γ coactivator (PGC1-1) and nuclear respiratory factor 2 (NRF-2). Our results suggest that Chlorella sorokiniana dietary supplementation has beneficial effects in counteracting oxidative stress and that it works primarily by preserving mitochondrial function. Thus, it can be useful in preventing dysfunctions in which mitochondrial oxidative damage and ROS production play a putative role.

Report this publication

Statistics

Seen <100 times