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Hydrogen sulfide (H2S), the third gasotransmitter, has positive roles in animals and plants. Mitochondria are the source and the target of H2S and the regulatory hub in metabolism, stress, and disease. Mitochondrial bioenergetics is a vital process that produces ATP and provides energy to support the physiological and biochemical processes. H2S regulates mitochondrial bioenergetic functions and mitochondrial oxidative phosphorylation. The article summarizes the recent knowledge of the chemical and biological characteristics, the mitochondrial biosynthesis of H2S, and the regulatory effects of H2S on the tricarboxylic acid cycle and the mitochondrial respiratory chain complexes. The roles of H2S on the tricarboxylic acid cycle and mitochondrial respiratory complexes in mammals have been widely studied. The biological function of H2S is now a hot topic in plants. Mitochondria are also vital organelles regulating plant processes. The regulation of H2S in plant mitochondrial functions is gaining more and more attention. This paper mainly summarizes the current knowledge on the regulatory effects of H2S on the tricarboxylic acid cycle (TCA) and the mitochondrial respiratory chain. A study of the roles of H2S in mitochondrial respiration in plants to elucidate the botanical function of H2S in plants would be highly desirable. [ABSTRACT FROM AUTHOR]

This study assessed the consequence of exposure to a pyrethroid insecticide, fenpropathrin (FPN), on the heart and the probable underlying mechanisms in rats. Moreover, the probable protective effect of curcumin-loaded chitosan nanoparticles (CMN-CNP) was evaluated. Forty male Sprague Dawley rats were distributed into four groups orally given corn oil, CMN-CNP (50 mg/kg b.wt), FPN (15 mg/kg b.wt), or CMN-CNP + FPN for 60 days. The results revealed that FPN exposure increased serum cardiac damage indicators. In addition, a substantial increase in the reactive oxygen species and malondialdehyde content but reduced enzymatic and non-enzymatic antioxidants and altered architecture was recorded in the cardiac tissue of FPN-exposed rats. Additionally, a significant down-regulation of expression of the mitochondrial complexes I–V, mitochondrial dynamics, and antioxidants-related genes but up-regulation of apoptosis-related genes was detected in the FPN-exposed group. Immunofluorescence analyses revealed higher amounts of the harmful protein 4-hydroxynonenal in the heart tissue of FPN-exposed rats. Nevertheless, the earlier disturbances were significantly rescued in the FPN + CMN-CNP treated group. Conclusively, our findings reported the cardiotoxic activity of FPN and the involvement of several mitochondrial imbalances as a probable underlying mechanism. Also, the study findings proved the efficacy of CMN-CNP in combating FPN cardiotoxic effects. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S), the third gasotransmitter, has positive roles in animals and plants. Mitochondria are the source and the target of H2S and the regulatory hub in metabolism, stress, and disease. Mitochondrial bioenergetics is a vital process that produces ATP and provides energy to support the physiological and biochemical processes. H2S regulates mitochondrial bioenergetic functions and mitochondrial oxidative phosphorylation. The article summarizes the recent knowledge of the chemical and biological characteristics, the mitochondrial biosynthesis of H2S, and the regulatory effects of H2S on the tricarboxylic acid cycle and the mitochondrial respiratory chain complexes. The roles of H2S on the tricarboxylic acid cycle and mitochondrial respiratory complexes in mammals have been widely studied. The biological function of H2S is now a hot topic in plants. Mitochondria are also vital organelles regulating plant processes. The regulation of H2S in plant mitochondrial functions is gaining more and more attention. This paper mainly summarizes the current knowledge on the regulatory effects of H2S on the tricarboxylic acid cycle (TCA) and the mitochondrial respiratory chain. A study of the roles of H2S in mitochondrial respiration in plants to elucidate the botanical function of H2S in plants would be highly desirable.

Blue-breasted quail has been recognized as a potential model animal. The aim of this study is to investigate the low-temperature-induced embryonic diapause in blue-breasted quail. To this end, the early embryonic staging in blue-breasted quail was briefly described and various incubation temperatures were tested. While the embryonic diapause in early blue-breasted quail embryos can be induced when the eggs were stored at 21°C, a lower temperature such as 16°C yielded a significantly better hatchability (P = 0.0231). Additionally, prolonged storage duration from 3, 7 to 14 d significantly reduced the hatchability (P < 0.0001). Visual examination on the unhatched eggs revealed that reduced hatchability in prolonged storage was significantly correlated with embryonic mortality during the first half of incubation period (R2 = 0.9999, P = 0.0055). High-throughput RNA sequencing with de novo assembly showed that a gene network cluster consisted of ND4, ND5, ND6 , and COX3 , which are components of mitochondrial respiratory complexes, was down-regulated in the cold-stored embryos, while a stress-responsive gene network cluster consisted of JUN, ATF3 , and DUSP1 was up-regulated. Accordingly, cell death in the blastoderm was significantly increased as the storage duration prolonged from 3 to 10 d. Taken together, our study provided basic information on the temperature-induced embryonic diapause in blue-breasted quail. Furthermore, transcriptomic analysis sheds light for the molecular basis on how blastoderm cells respond to the prolonged cold-stress and stay diapause. [ABSTRACT FROM AUTHOR]

The purpose of this study was to set up a beagle dog model, for radiation-induced lung injury, that would be able to supply fresh lung tissues in the different injury phases for research into oxidative stress levels and mitochondrial gene expression. Blood serum and tissues were collected via CT-guided core needle biopsies from dogs in the various phases of the radiation response over a 40-week period. Levels of reactive oxygen species (ROS) and manganese superoxide dismutase 2 (MnSOD) protein expression in radiation-induced lung injury were determined by in situ immunocytochemistry; malondialdehyde (MDA) content and reductase activity in the peripheral blood were also tested; in addition, the copy number of the mitochondrial DNA and the level of function of the respiratory chain in the lung tissues were assessed. ROS showed dynamic changes and peaked at 4 weeks; MnSOD was mainly expressed in the Type II alveolar epithelium at 8 weeks; the MDA content and reductase activity in the peripheral blood presented no changes; the copy numbers of most mitochondrial genes peaked at 8 weeks, similarly to the level of function of the corresponding respiratory chain complexes; the level of function of the respiratory chain complex III did not peak until 24 weeks, similarly to the level of function of the corresponding gene Cytb. Radiation-induced lung injury was found to be a dynamically changing process, mainly related to interactions between local ROS, and it was not associated with the levels of oxidative stress in the peripheral blood. Mitochondrial genes and their corresponding respiratory chain complexes were found to be involved in the overall process. [ABSTRACT FROM AUTHOR]

Complex II (succinate dehydrogenase) is an essential mitochondrial enzyme involved in both the tricarboxylic acid cycle and the respiratory chain. In Arabidopsis thaliana, its iron-sulfur subunit (SDH2) is encoded by three genes, one of them (SDH2.3) being specifically expressed during seed maturation in the embryo. Here we show that seed SDH2.3 expression is regulated by abscisic acid (ABA) and we define the promoter region (-114 to C49) possessing all the cis-elements necessary and sufficient for high expression in seeds. This region includes between -114 and -32 three ABRE (ABA-responsive) elements and one RY-enhancer like element, and we demonstrate that these elements, although necessary, are not sufficient for seed expression, our results supporting a role for the region encoding the 5' untranslated region (C1 to C49). The SDH2.3 promoter is activated in leaf protoplasts by heterodimers between the basic leucine zipper transcription factors bZIP53 (group S1) and bZIP10 (group C) acting through the ABRE elements, and by the B3 domain transcription factor ABA insensitive 3 (ABI3). The in vivo role of bZIP53 is further supported by decreased SDH2.3 expression in a knockdown bzip53 mutant. By using the protein synthesis inhibitor cycloheximide and sdh2 mutants we have been able to conclusively show that complex II is already present in mature embryos before imbibition, and contains mainly SDH2.3 as iron-sulfur subunit. This complex plays a role during seed germination sensu-stricto since we have previously shown that seeds lacking SDH2.3 show retarded germination and now we demonstrate that low concentrations of thenoyltrifluoroacetone, a complex II inhibitor, also delay germination. Furthermore, complex II inhibitors completely block hypocotyl elongation in the dark and seedling establishment in the light, highlighting an essential role of complex II in the acquisition of photosynthetic competence and the transition from heterotrophy to autotrophy. [ABSTRACT FROM AUTHOR]

J. Neurochem. (2010) 114, 130–141. Ketones have previously shown beneficial effects in models of neurodegenerative disorders, particularly against associated mitochondrial dysfunction and cognitive impairment. However, evidence of a synaptic protective effect of ketones remains lacking. We tested the effects of ketones on synaptic impairment induced by mitochondrial respiratory complex (MRC) inhibitors using electrophysiological, reactive oxygen species (ROS) imaging and biochemical techniques. MRC inhibitors dose-dependently suppressed both population spike (PS) and field potential amplitudes in the CA1 hippocampus. Pre-treatment with ketones strongly prevented changes in the PS, whereas partial protection was seen in the field potential. Rotenone (Rot; 100 nmol/L), a MRC I inhibitor, suppressed synaptic function without altering ROS levels and PS depression by Rot was unaffected by antioxidants. In contrast, antioxidant-induced PS recovery against the MRC II inhibitor 3-nitropropionic acid (3-NP; 1 mmol/L) was similar to the synaptic protective effects of ketones. Ketones also suppressed ROS generation induced by 3-NP. Finally, ketones reversed the decreases in ATP levels caused by Rot and 3-NP. In summary, our data demonstrate that ketones can preserve synaptic function in CA1 hippocampus induced by MRC dysfunction, likely through an antioxidant action and enhanced ATP generation. [ABSTRACT FROM AUTHOR]

Abstract: In order to investigate the effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, production of reactive oxygen species (ROS) and lipid peroxidation in broiler chickens, 128 six-week-old broiler chickens were kept in a controlled-environment chamber. The broiler chickens were initially kept at 25°C (relative humidity, RH, 70±5%) for 6d and subsequently exposed to 35°C (RH, 70±5%) for 3h, then the heat stress was removed and the temperature returned to 25°C (RH, 70±5%). Blood and liver samples were obtained before heat exposure and at 0 (at the end of the three-hour heating episode, this group is also abbreviated as the HT group), 1, 2, 4, 8, 12h after the stress was removed. The results showed that acute heat stress induced a significant production of ROS, function of the mitochondrial respiratory chain, antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activity, and formation of malondialdehybe (MDA). Within the first 12h after removal of the heat stress, the acute modification of the above parameters induced by heat stress gradually approached to pre-heat levels. The results of the present study suggest that acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This leads to over-production of ROS, which ultimately results in lipid peroxidation and oxidative stress. When the high temperature was removed, the production of ROS, mitochondrial respiratory function and oxidative injury that were induced by acute heat exposure gradually approached the levels observed before heating, in a time-dependent manner. [Copyright &y& Elsevier]

• HIIT have negative effects on the plasticity of the hippocampus in middle-aged mice. • HIIT decrease of the expression of p-CREB and BDNF in middle-aged mice hippocampus. • HIIT have a complex influence in mitochondrial respiratory chain of middle-aged mice. • HIIT may inhibit mitophagy in middle-aged mice hippocampus. Autophagy is involved in aging-related cognitive impairment. Aerobic exercise training can improve cognitive function in the elderly and this effect may be associated with autophagic mechanisms and mitochondrial respiratory function. High intensity interval training (HIIT) has beneficial effects on heart and skeletal muscles by activating autophagy and/or mitophagy, but the effects of HIIT on autophagy/mitophagy in the aging brain are unknown. This study investigated the effects of HIIT on the mitochondrial respiratory complex and autophagy/mitophagy, and its relation to brain function. Thirteen middle-aged male ICR mice underwent HIIT for 7 weeks. The exercise program reduced the spontaneous behavior and exploration activities of the mice. The phosphorylation level of cAMP response element binding protein (CREB) and the protein expression of brain-derived neurotrophic factor (BDNF) decreased after the 7-week HIIT. Exercise downregulated the protein expression of Complex Ⅰ and upregulated the protein expression of Complex Ⅲ, Complex Ⅳ and Complex Ⅴ. HIIT also decreased the expression of mitophagy-related proteins in the mitochondrial fractions of the hippocampus. However, HIIT did not change the expression of autophagy-related proteins LC3, P62, Atg5, Atg7, Beclin-1 and Lamp2 in the total lysate of the hippocampus. These data indicated that HIIT might have negative effects on the plasticity of the hippocampus in middle-aged mice. The effects may be related to the dysregulation of CREB-BDNF signaling, mitochondrial respiratory complex and mitophagy induced by HIIT. [ABSTRACT FROM AUTHOR]

[Display omitted] • ATP export in leaves under ultraviolet-B radiation required mitochondrial regulation. • Increase of geranylgeranyl pyrophosphate synthase promoted alkaloid biosynthesis. • Increase of eight alkaloids in response to ultraviolet-B radiation were detected. Indole alkaloids from Catharanthus roseus (L.) G. Don were valued for their wide spectrum of pharmaceutical effects. Their biosynthesis is modulated by various abiotic factors including ultraviolet B radiation which induced ATP production and led to accumulation of indole alkaloids. To investigate the regulatory mechanism of secondary metabolism in the leaf mitochondria of C. roseus under ultraviolet B radiation, combinatory study of proteomic and metabolomic analyses of C. roseus was performed. ATP export in the leaves of C. roseus increased under UVB radiation, which required mitochondrial ATP synthase. Proteins related to mitochondrial complexes II/IV and their gene expression levels increased, and those related to mitochondrial complex I decreased. Proteins related to the methylerythritol phosphate pathway, especially geranylgeranyl pyrophosphate synthase, increased under ultraviolet B radiation. Metabolites whose levels changed were mainly alkaloids, organic acids, carbohydrates, phenylpropanoids, and fatty acids, while eight indole alkaloids increased. Integrative analysis of omics data indicated that the metabolism of glutamate and tyrosine was downregulated. These results suggest that ultraviolet B radiation induces dynamic changes in mitochondria in C. roseus , which guarantees ATP production, regulates the flux of the methylerythritol phosphate pathway to the biosynthesis of monoterpene moieties, and leads to accumulation of various indole alkaloids. [ABSTRACT FROM AUTHOR]

Hyperglycemia induces nonconcordant regulation of renal mitochondrial respiratory complexes, increases oxidative stress, and causes diabetic nephropathy. Hypertension is a complication associated with diabetes and involves glomerular hyperfiltration, the effects of which on mitochondrial respiratory complexes are not well understood. To investigate the effect of glomerular hyperfiltration on renal mitochondrial respiratory complexes, we used the 5/6 nephrectomized BKS. Cg-Dock7 m +/+Lepr db /J, Dock7 m +/+Lepr db mice (db/m-5/6Nx mice) as a model for glomerular hyperfiltration. The BKS. Cg-Dock7 m +/+Lepr db /J, +Lepr db /+Lepr db mice (db/db mice), a model for type 2 diabetes, was used as the positive control. We investigated the activities and protein levels of the mitochondrial complex, and the mitochondrial DNA and adenosine triphosphate content in the kidneys of these models. Blood chemistry and renal histopathological examination were performed for characterization of the disease. Both models showed expansion of the mesangial matrix of the glomeruli, which is indicative of glomerular hyperfiltration. The activities of complexes I and IV and the protein levels of complexes I and III were nonconcordant in db/m-5/6Nx mice. In conclusion, we demonstrated that nonconcordant regulation of mitochondrial complexes in db/m-5/6Nx mice involved with glomerular hyperfiltration. The progression and/or severity of nephropathy might be affected through a synergistic effect of mitochondrial dysfunction in hyperglycemia and glomerular hyperfiltration. J. Med. Invest. 64: 255-261, August, 2017.

Mitochondria actively participate in neurotransmission by providing energy (ATP) and maintaining normative concentrations of reactive oxygen species (ROS) in both presynaptic and postsynaptic elements. In human and animal epilepsies, ATP-producing respiratory rates driven by mitochondrial respiratory complex (MRC) I are reduced, antioxidant systems are attenuated and oxidative damage is increased. We report that MRCI-driven respiration and functional uncoupling (an inducible antioxidant mechanism) are reduced and levels of H2O2 are elevated in mitochondria isolated from KO mice. Experimental impairment of MRCI in WT hippocampal slices via rotenone reduces paired-pulse ratios (PPRs) at mossy fiber-CA3 synapses (resembling KO PPRs), and exacerbates seizure-like events in vitro. Daily treatment with AATP [a combination therapy composed of ascorbic acid (AA), alpha-tocopherol (T), sodium pyruvate (P) designed to synergistically target mitochondrial impairments] improved mitochondrial functions, mossy fiber PPRs, and reduced seizure burden index (SBI) scores and seizure incidence in KO mice. AATP pretreatment reduced severity of KA-induced seizures resulting in 100% protection from the severe tonic-clonic seizures in WT mice. These data suggest that restoration of bioenergetic homeostasis in the brain may represent a viable anti-seizure target for temporal lobe epilepsy., (Copyright © 2013 Elsevier Inc. All rights reserved.)