Propagation of Mitochondria-Derived Reactive Oxygen Species within the Dipodascus magnusii Cells

Abstract

Mitochondria are considered to be the main source of reactive oxygen species (ROS) in the cell. It was shown that in cardiac myocytes exposed to excessive oxidative stress, ROS-induced ROS release is triggered. However, cardiac myocytes have a network of densely packed organelles that do not move, which is not typical for the majority of eukaryotic cells. The purpose of this study was to trace the spatiotemporal development (propagation) of prooxidant-induced oxidative stress and its interplay with mitochondrial dynamics. We used Dipodascus magnusii yeast cells as a model, as they have advantages over other models, including a uniquely large size, mitochondria that are easy to visualize and freely moving, an ability to vigorously grow on well-defined low-cost substrates, and high responsibility. It was shown that prooxidant-induced oxidative stress was initiated in mitochondria, far preceding the appearance of generalized oxidative stress in the whole cell. For yeasts, these findings were obtained for the first time. Preincubation of yeast cells with SkQ1, a mitochondria-addressed antioxidant, substantially diminished production of mitochondrial ROS, while only slightly alleviating the generalized oxidative stress. This was expected, but had not yet been shown. Importantly, mitochondrial fragmentation was found to be primarily induced by mitochondrial ROS preceding the generalized oxidative stress development.

Altered Mitochondrial Morphology and Bioenergetics in a New Yeast Model Expressing Aβ42

“…Preincubation of these strains with 250 nM SkQThy for 1 h noticeably decreased oxidative stress and significantly increased the viability of the cells. Incubation for 2 h of both strains with t-BHP [ 63 ] expectedly increased oxidative stress while decreasing the viability. When preincubation with SkQThy preceded the treatment with the prooxidant, the positive effect of SkQThy was noticeable and reproducible.…”

“…Mitochondria are critical for cell survival and death. In addition to their well-known energy storage function, they are deeply integrated into the cellular metabolism, required for growth and proliferation; implicated in modulating cell signaling, maintaining redox homeostasis, and regulating cell adaption to external stress factors and apoptosis (reviewed in [ 63 ]). To fulfill their energy needs, neurons, post-mitotic and excitable cells, rely almost exclusively on the mitochondrial oxidative phosphorylation system.…”

Nanosheets Based Approach to Elevate the Proliferative and Differentiation Efficacy of Human Wharton’s Jelly Mesenchymal Stem Cells

“…Furthermore, the impact of nanosheet exposure on the mitochondria activity of hWJ-MSCs was investigated. The mitochondria are multipurpose organelles with various cellular functions [ 30 , 31 ], such as being the primary producer of ROS, and they play a critical role in the physiological and pathophysiological processes including cancer development, immune functions, and blood glucose control [ 30 , 31 , 32 ]. Mitochondrial ROS (mtROS) of the treated cells were measured using the MitoSOX Red reagent [ 33 ].…”

Mitochondrial Targeted Antioxidant SKQ1 Ameliorates Acute Kidney Injury by Inhibiting Ferroptosis

“…SKQ1 is known as a mitochondria-targeting antioxidant capable of scavenging ROS and oxygen free radicals in a variety of diseases [ 51 ]. In the present study, while the RNA sequencing analysis showed that ferroptotic signaling was one of the chief downregulated pathways after treatment with SKQ1, we noted that the other pathways of apoptosis, necroptosis, and inflammation were also downregulated after SKQ1 treatment in mice.…”