In Rhodotorula mucilaginosa, active oxidative metabolism increases carotenoids to inactivate excess reactive oxygen species
Por:
Mosqueda-Martínez, E, Chiquete-Félix, N, Castañeda-Tamez, P, Ricardez-García, C, Gutiérrez-Aguilar, M, Uribe-Carvajal, S, Mendez-Romero, O
Publicada:
6 sep 2024
Resumen:
Carotenoids produced by bacteria, yeasts, algae and plants inactivate Free Radicals (FR). However, FR may inactivate carotenoids and even turn them into free radicals. Oxidative metabolism is a source of the highly motile Reactive Oxygen Species (ROS). To evaluate carotenoid interactions with ROS, the yeast Rhodotorula mucilaginosa was grown in dextrose (YPD), a fermentative substrate where low rates of oxygen consumption and low carotenoid expression were observed, or in lactate (YPLac), a mitochondrial oxidative-phosphorylation (OxPhos) substrate, which supports high respiratory activity and carotenoid production. ROS were high in YPLac-grown cells and these were unmasked by the carotenoid production-inhibitor diphenylamine (DPA). In contrast, in YPD-grown cells ROS were almost absent. It is proposed that YPLac cells are under oxidative stress. In addition, YPLac-grown cells were more sensitive than YPD-grown cells to menadione (MD), a FR-releasing agent. To test whether carotenoids from cells grown in YPLac had been modified by ROS, carotenoids from each, YPD- and YPLac-grown cells were isolated and added back to cells, evaluating protection from MD. Remarkably, carotenoids extracted from cells grown in YPLac medium inhibited growth, while in contrast extracts from YPD-grown cells were innocuous or mildly protective. Results suggest that carotenoid-synthesis in YPLac-cells is a response to OxPhos-produced ROS. However, upon reacting with FR, carotenoids themselves may be inactivated or even become prooxidant themselves.
Filiaciones:
Univ Nacl Autonoma Mexico, Dept Genet & Mol Biol, Inst Fisiol Celular, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Fac Quim, Dept Biochem, Mexico City, Mexico
gold, All Open Access; Gold Open Access
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