Effect of hypothermia on the functional activity of liver mitochondria of grass snake (Natrix natrix): inhibition of succinate-fueled respiration and K+ transport, ROS-induced activation of mitochondrial permeability transition

Dubinin, Mikhail V.; Svinin, Anton O.; Vedernikov, A. A.; Starinets, Vlada S.; Tenkov, Kirill S.; Belosludtsev, Konstantin N.; Самарцев, В. Н.

doi:10.1007/s10863-019-09796-6

Cited by 16 publications

(4 citation statements)

References 51 publications

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“…These molecules contribute to various cell structures and biological processes, influencing membrane composition, signal transduction, cell division, and regulation of lipid metabolism, among others [11]. Moreover, PUFAs serve as energy sources and regulate the phospholipid composition of mitochondrial membranes [12]. FADS1 localizes to the endoplasmic reticulum and mitochondria [13].…”

Section: Introductionmentioning

confidence: 99%

Suppression of FADS1 induces ROS generation, cell cycle arrest, and apoptosis in melanocytes: implications for vitiligo

Tang

et al. 2019

Aging

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Vitiligo is a potentially serious condition characterized by loss of melanin and death of melanocytes. To identify potential therapeutic targets for vitiligo, we conducted a microarray analysis of three human vitiligo specimens and paired adjacent normal tissues. Because we found that the fatty acid desaturase 1 (FADS1) gene was downregulated in vitiligo specimens, we carried out experiments to assess its role in melanocyte replication and survival. RT-qPCR was used to verify that FADS1 expression was lower in vitiligo-affected tissues and vitiligo melanocyte PIG3V cells than in matched controls or normal human epidermal PIG1 melanocytes. In addition, CCK-8, immunofluorescence, western blot and flow cytometry assay were used to detect the proliferation and apoptosis in PIG1 cells respectively. Overexpression of FADS1 promoted proliferation of PIG3V melanocytes, while FADS1 silencing inhibited proliferation and induced cell death in PIG1 melanocytes. Increased ROS generation; induction of mitochondrial-mediated apoptosis via upregulation of Bax and active caspases 3 and 9 and downregulation of Bcl-2; and cell cycle arrest via downregulation of c-Myc and Cyclin D1 and upregulation of p21 were all enhanced after FADS1 silencing in PIG1 melanocytes. These findings implicate FADS1 downregulation in the pathogenesis of vitiligo and may open new avenues for its treatment.

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Section: Introductionmentioning

confidence: 99%

Suppression of FADS1 induces ROS generation, cell cycle arrest, and apoptosis in melanocytes: implications for vitiligo

Tang

et al. 2019

Aging

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“…Unfortunately, mitochondrial function studies in snakes are scarce. Interestingly, it was found that low temperature can impact coupling and efficiency in liver mitochondria of the snake Natrix natrix , but only when respiration was driven by succinate as the respiratory substrate (Dubinin et al, 2019), indicating that different sources of stimulus can impact mitochondrial function distinctly.…”

Section: Discussionmentioning

confidence: 99%

Feeding effects on liver mitochondrial bioenergetics of Boa constrictor (Serpentes: Boidae)

Araujo

Sartori

Navarro

et al. 2021

Preprint

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Snakes are interesting examples of overcoming energy metabolism challenges as many species can endure long periods without feeding, and their eventual meals are of reasonably large sizes, thus exhibiting dual extreme adaptations. Consequently, metabolic rate increases considerably to attend to the energetic demand of digestion, absorption and, protein synthesis. These animals should be adapted to transition from these two opposite states of energy fairly quickly, and therefore we investigated mitochondrial function plasticity in these states. Herein we compared liver mitochondrial bioenergetics of the boid snake Boa constrictor during fasting and after meal intake. We fasted the snakes for 60 days, then we fed a subgroup with 30% of their body size and evaluated their maximum postprandial response. We measured liver respiration rates from permeabilized tissue and isolated mitochondria, and from isolated mitochondria, we also measured Ca2+ retention capacity, the release of H2O2, and NAD(P) redox state. Mitochondrial respiration rates were maximized after feeding, reaching until 60% increase from fasting levels when energized with complex I-linked substrates. Interestingly, fasting and fed snakes exhibited similar respiratory control ratios and citrate synthase activity. Furthermore, we found no differences in Ca2+ retention capacity, indicating no increase in susceptibility to mitochondrial permeability transition pore (PTP), or redox state of NAD(P), although fed animals exhibited increases in the release of H2O2. Thus, we conclude that liver mitochondria from B. constrictor snakes increase the maintenance costs during the postprandial period and quickly improve the mitochondrial bioenergetics capacity without compromising the redox balance.

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“…The rate of H 2 O 2 production by the suspension of rat liver mitochondria was measured with the fluorescent indicator Amplex Red (λ ex = 560 nm; λ em = 590 nm) using Fluorat-02-Panorama spectrofluorimeter (Lumex Instruments, St. Petersburg, Russia) at 37 °C [ 32 ]. Rat liver mitochondria (0.15 mg/mL) were incubated in the medium containing 210 mM mannitol, 70 mM sucrose, 1 mM KH 2 PO 4 , 10 μM EGTA, and 10 mM Hepes/KOH buffer, pH 7.4.…”

Section: Methodsmentioning

confidence: 99%

Effect of F16-Betulin Conjugate on Mitochondrial Membranes and Its Role in Cell Death Initiation

et al. 2021

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This work demonstrates the effects of a newly synthesized conjugate of the plant triterpenoid betulin and the penetrating cation F16 used for mitochondrial targeting. The resulting F16-betulin conjugate revealed a mitochondria-targeted effect, decreasing the mitochondrial potential and inducing superoxide overproduction in rat thymocytes in vitro. It has been suggested that this may cause the cytotoxic effect of the conjugate, which significantly exceeds the effectiveness of its precursors, betulin and F16. Using isolated rat liver mitochondria, we found that the F16-betulin conjugate has a surface-active effect on mitochondrial membranes, causing organelle aggregation. This effect of the derivative resulted in a dose-dependent decrease in mitochondrial transmembrane potential, as well as suppression of respiration and oxidative phosphorylation, especially in the case of nicotinamide adenine dinucleotide (NAD)-fueled organelles. In addition, the F16-betulin conjugate caused an increase in H2O2 generation by mitochondria fueled with glutamate and malate. These effects of the derivative can presumably be due to the powerful suppression of the redox activity of complex I of the mitochondrial electron transport chain. The paper discusses how the mitochondria-targeted effects of the F16-betulin conjugate may be related to its cytotoxic effects.

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Effect of hypothermia on the functional activity of liver mitochondria of grass snake (Natrix natrix): inhibition of succinate-fueled respiration and K+ transport, ROS-induced activation of mitochondrial permeability transition

Cited by 16 publications

References 51 publications

Suppression of FADS1 induces ROS generation, cell cycle arrest, and apoptosis in melanocytes: implications for vitiligo

Suppression of FADS1 induces ROS generation, cell cycle arrest, and apoptosis in melanocytes: implications for vitiligo

Feeding effects on liver mitochondrial bioenergetics of Boa constrictor (Serpentes: Boidae)

Effect of F16-Betulin Conjugate on Mitochondrial Membranes and Its Role in Cell Death Initiation

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