Role of mitochondrial calcium transport in the control of substrate oxidation

1998 ◽  
pp. 359-369 ◽  
Author(s):  
Richard G. Hansford ◽  
Dmitry Zorov
Keyword(s):  
Calcium Transport ◽  
Substrate Oxidation ◽  
Mitochondrial Calcium

scholarly journals Role of Polyhydroxybutyrate in Mitochondrial Calcium Transport

2012 ◽  
Vol 102 (3) ◽  
pp. 165a
Author(s):  
Matthew Smithen ◽  
Pia Elustondo ◽  
Robert Winkfein ◽  
Eleonora Zakharian ◽  
Andrey Abramov ◽  
...  
Keyword(s):  
Calcium Transport ◽  
Mitochondrial Calcium

Role of mitochondrial calcium transport for myocardial hypermetabolism during reperfusion

1990 ◽  
Vol 22 ◽  
pp. S107 ◽  
Author(s):  
René Lerch ◽  
Irene Papageorgiou ◽  
Eugenia Marquez ◽  
Richard Benzi
Keyword(s):  
Calcium Transport ◽  
Mitochondrial Calcium

Excitation–contraction coupling in heart. XIX. Effect of hypoxia on calcium transport by subcellular particles in the isolated perfused rat heart

1976 ◽  
Vol 54 (1) ◽  
pp. 49-58 ◽  
Author(s):  
S. L. Lee ◽  
V. Balasubramanian ◽  
N. S. Dhalla
Keyword(s):  
Calcium Binding ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Microsomal Fraction ◽  
Contractile Force ◽  
Mitochondrial Calcium ◽  
Rat Hearts ◽  
Mitochondrial Calcium Uptake ◽  
Contractile Failure

To examine the role of changes in calcium transport by subcellular particles in the pathogenesis of contractile failure due to oxygen lack, both mitochondrial and microsomal fractions were obtained from the isolated hypoxic rat hearts and their calcium binding and uptake abilities were determined by the Millipore filtration technique. The contractile force decreased by about 40, 60 and 70% of the control within 5, 10 and 30 min respectively, of perfusing the heart with hypoxic medium containing glucose. In hearts perfused for 10 min with hypoxic medium containing glucose, calcium binding and uptake by the microsomal fraction decreased significantly. However, mitochondrial calcium binding, but not uptake, decreased significantly on perfusing the hearts with hypoxic medium containing glucose for 20 to 30 min when the microsomal calcium transport was markedly depressed. Reduction in contractile force, calcium binding and uptake by the microsomal fraction as well as calcium binding by mitochondria of hearts made hypoxic for 30 min recovered towards normal upon reperfusion with control medium for 15 min. On the other hand, omitting glucose from the hypoxic medium significantly decreased calcium binding by mitochondrial and microsomal fractions within 10 min of perfusion in comparison to the control and accelerated the effects of hypoxia upon contractile force and microsomal calcium uptake. In contrast to the hypoxic hearts, the mitochondrial calcium uptake decreased significantly and the magnitude of depression in the microsomal calcium binding was appreciably greater in hearts made to fail to a comparable degree upon perfusion with substrate-free medium. The observed defects in calcium transporting properties of microsomal and mitochondrial membranes appear secondary to the contractile failure in hypoxic hearts.

scholarly journals Oxidation of Terpenoids to Achieve High-Value Flavor and Fragrances—Questioning Microalgae Oxidative Capabilities in the Biotransformation of the Sesquiterpene Valencene and of Selected Natural Apocarotenoids

Chemistry ◽  
2021 ◽  
Vol 3 (3) ◽  
pp. 821-830
Author(s):  
Davide De Simeis ◽  
Stefano Serra ◽  
Alessandro Di Fonzo ◽  
Francesco Secundo
Keyword(s):  
Experimental Data ◽  
Natural Products ◽  
Aqueous Medium ◽  
Photochemical Reaction ◽  
Substrate Oxidation ◽  
Market Size ◽  
Chlorella Sp ◽  
General Opinion ◽  
Natural Way

Natural flavor and fragrance market size is expected to grow steadily due to the rising consumer demand of natural ingredients. This market request is guided by the general opinion that the production of natural compounds leads to a reduction of pollution, with inherent advantages for the environment and people’s health. The biotransformation reactions have gained high relevance in the production of natural products. In this context, few pieces of research have described the role of microalgae in the oxidation of terpenoids. In this present study, we questioned the role of microalgal based oxidation in the synthesis of high-value flavors and fragrances. This study investigated the role of three different microalgae strains, Chlorella sp. (211.8b and 211.8p) and Chlorococcum sp. (JB3), in the oxidation of different terpenoid substrates: α-ionone, β-ionone, theaspirane and valencene. Unfortunately, the experimental data showed that the microalgal strains used are not responsible for the substrate oxidation. In fact, our experiments demonstrate that the transformation of the four starting compounds is a photochemical reaction that involves the oxygen as oxidant. Even though these findings cast a shadow on the use of these microorganisms for an industrial purpose, they open a new possible strategy to easily obtain nootkatone in a natural way by just using an aqueous medium, oxygen and light.

scholarly journals ApoE4 (Δ272–299) induces mitochondrial‐associated membrane formation and mitochondrial impairment by enhancing GRP75-modulated mitochondrial calcium overload in neuron

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tao Liang ◽  
Weijian Hang ◽  
Jiehui Chen ◽  
Yue Wu ◽  
Bin Wen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Calcium Transport ◽  
Calcium Overload ◽  
Mitochondrial Calcium ◽  
Mitochondrial Impairment

Abstract Background Apolipoprotein E4 (apoE4) is a major genetic risk factor of Alzheimer’s disease. Its C-terminal-truncated apoE4 (Δ272–299) has neurotoxicity by affecting mitochondrial respiratory function. However, the molecular mechanism(s) underlying the action of apoE4 (Δ272–299) in mitochondrial function remain poorly understood. Methods The impact of neuronal apoE4 (Δ272–299) expression on ER stress, mitochondrial-associated membrane (MAM) formation, GRP75, calcium transport and mitochondrial impairment was determined in vivo and in vitro. Furthermore, the importance of ER stress or GRP75 activity in the apoE4 (Δ272–299)-promoted mitochondrial dysfunction in neuron was investigated. Results Neuronal apoE4 (Δ272–299) expression induced mitochondrial impairment by inducing ER stress and mitochondrial-associated membrane (MAM) formation in vivo and in vitro. Furthermore, apoE4 (Δ272–299) expression promoted GRP75 expression, mitochondrial dysfunction and calcium transport into the mitochondria in neuron, which were significantly mitigated by treatment with PBA (an inhibitor of ER stress), MKT077 (a specific GRP75 inhibitor) or GRP75 silencing. Conclusions ApoE4 (Δ272–299) significantly impaired neuron mitochondrial function by triggering ER stress, up-regulating GRP75 expression to increase MAM formation, and mitochondrial calcium overload. Our findings may provide new insights into the neurotoxicity of apoE4 (Δ272–299) against mitochondrial function and uncover new therapeutic targets for the intervention of Alzheimer’s disease.

Inhibition of rat brain mitochondrial calcium transport by chlordecone

1979 ◽  
Vol 51 (1) ◽  
pp. 189-196 ◽  
Author(s):  
David W. End ◽  
Richard A. Carchman ◽  
Richard Ameen ◽  
William L. Dewey
Keyword(s):  
Rat Brain ◽  
Calcium Transport ◽  
Mitochondrial Calcium

Abstract 125: Perturbation of Mitochondrial Calcium Uniporter Promotes Cardiac Oxidative Stress and Autophagy During Heart Failure

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Sudarsan Rajan ◽  
Santhanam Shanmughapriya ◽  
Dhanendra Tomar ◽  
Zhiwei Dong ◽  
Joseph Y Cheung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Mouse Model ◽  
Atp Depletion ◽  
Regulatory Role ◽  
Mitochondrial Calcium ◽  
Mitochondrial Bioenergetics ◽  
Complex Assembly ◽  
New Findings

Mitochondrial calcium ([Ca 2+ ] m ) is essential for cardiomyocyte viability, and aberration of [Ca 2+ ] m is known to elicit multiple cardiac stress conditions associated with ATP depletion, reactive oxygen species, and mitochondrial permeability transition pore opening, all of which can lead to metabolic stress and the loss of dysfunctional mitochondria by aberrant autophagy. Elucidating the regulatory role of m itochondrial c alcium u niporter (MCU)-mediated [Ca 2+ ] m in modulating cardiac mitochondrial bioenergetics and autophagy has high significance and clinical impact for many pathophysiological processes. [Ca 2+ ] m is exquisitely controlled by the inner mitochondrial membrane uniporter, transporters, regulators and exchangers including MCU, MCUR1, EMRE, MICU1, MICU2 and LETM1. Our recently published findings revealed that Mitochondrial Ca 2+ Uniporter Regulator 1 (MCUR1) serves as a scaffold factor for uniporter complex assembly. We found that deletion of MCUR1 impaired [Ca 2+ ] m uptake, mitochondrial Ca 2+ current ( I MCU ) and mitochondrial bioenergetics and is associated with increased autophagy. Our new findings indicate that the impairment of [Ca 2+ ] m uptake exacerbated autophagy following ischemia-reperfusion (I/R) injury. In support of our mouse model, human failing hearts show that MCUR1 protein levels are markedly decreased and autophagy markers are increased, demonstrating a crucial link between [Ca 2+ ] m uptake and autophagy during heart failure. Additionally, our results reveal that either oxidation or disruption of human MCU Cys-97 (in mouse Cys-96; gain-of-function MCU C96A mutant) produces a conformational change within the N terminal β-grasp fold of MCU which promotes higher-order MCU complex assembly and increased I MCU activity and mitochondrial ROS levels. The results of our studies using a novel cardiac-specific MCUR1-KO model and a constitutively active global MCU C96A KI mouse model (CRISPR-Cas9 genome edited) elucidate the regulatory role of [Ca 2+ ] m in cardiac bioenergetics and autophagy during oxidative stress and myocardial infarction. Thus, targeting assembly and the activity of MCU complex will offer a new potential therapeutic target in the treatment of cardiomyopathy and heart failure.

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