bims-resufa 2021-12-12 papers

Issue of 2021‒12‒12
two papers selected by
Vera Strogolova
Strong Microbials, Inc

J Gerontol A Biol Sci Med Sci. 2021 Dec 06. pii: glab363. [Epub ahead of print]

Supercomplex organization of the electron transfer system in marine bivalves, a model of extreme longevity.

Enrique Rodríguez, Amanda Radke, Tory M Hagen, Pierre U Blier.

The mitochondrial oxidative stress theory of aging (MOSTA) suggests that the organelle's decay contributes to the aging phenotype via exacerbated oxidative stress, loss of organ coordination and energetics, cellular integrity and activity of the mitochondrial electron transfer system (ETS). Recent advances in understanding the structure of the ETS show that the enzymatic complexes responsible for oxidative phosphorylation are arranged in supramolecular structures called supercomplexes that lose organization during aging. Their exact role and universality among organisms are still under debate. Here, we take advantage of marine bivalves as an aging model to compare the structure of the ETS among species ranging from 28 to 507 years in maximal lifespan. Our results show that regardless of lifespan, the bivalve ETS is arrayed as a set of supercomplexes. However, bivalve species display varying degrees ETS supramolecular organization with the highest supercomplex structures found in A. islandica, the longest-lived of the bivalve species under study. We discuss this comparative model in light of differences in the nature and stoichiometry of these complexes, and highlight the potential link between the complexity of these superstructures and longer lifespans.

Keywords: Electron transfer system; Invertebrate; Mitochondria; Supercomplex

DOI: https://doi.org/10.1093/gerona/glab363

J Hazard Mater. 2022 Feb 15. pii: S0304-3894(21)02514-0. [Epub ahead of print]424(Pt B): 127546

Thorium inhibits human respiratory chain complex IV (cytochrome c oxidase).

Libing Yu, Zhaozhu Lin, Xuedan Cheng, Jian Chu, Xijian Li, Chun Chen, Tinghua Zhu, Wenjing Li, Wei Lin, Wei Tang.

Thorium is a radioactive heavy metal and an emerging environmental pollutant. Ecological and human health risks from thorium exposure are growing with the excavation of rare earth metals and implementation of thorium-based nuclear reactors. Thorium poisoning is associated with carcinogenesis, liver impairments, and congenital anomalies. To date, the biomolecular targets that underlie thorium-induced toxicity remain unknown. Here, we used in vitro enzymatic activity assays to comprehensively evaluate the effects of thorium on the mitochondrial respiration process. Thorium was found to inhibit respiratory chain complex IV (cytochrome c oxidase) at sub-micromolar concentrations (IC50 ~ 0.4 μM, 90 μg/L). This is lower than the thorium level limit (246 μg/L) in drinking water specified by the World Health Organization. The inhibitory effects were further verified in mitochondria from human bone and liver cells (thorium mainly deposits in these organs). The inhibition of cytochrome c oxidase can readily rationalize well-documented cellular toxicities of thorium, such as alteration of mitochondrial membrane potential and production of reactive oxygen species. Therefore, cytochrome c oxidase is potentially a key molecular target underlying thorium-induced toxicological effect.

Keywords: CcO; Cytochrome c oxidase; Respiratory chain complex; Thorium; Toxicology

DOI: https://doi.org/10.1016/j.jhazmat.2021.127546