Electron Transport Complex I

Publication Title: 
International Journal of Nanomedicine

Platinum nanoparticle (Pt-np) species are superoxide dismutase/catalase mimetics and also have an activity similar to that of mitochondrial electron transport complex I. To examine if this complex I-like activity functions in vivo, we studied the effects of Pt-nps on the lifespan of a mitochondrial complex I-deficient Caenorhabditis elegans mutant, nuo-1 (LB25) compared with wild-type N2. We synthesized a fusion protein of a cell-penetrating peptide, human immunodeficiency virus-1 TAT (48-60), C-terminally linked to a peptide with a high affinity to platinum (GRKKRRQRRRPPQ-DRTSTWR).

Author(s): 
Sakaue, Yuri
Kim, Juewon
Miyamoto, Yusei
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

There is an urgent need for new antimalarial drugs with novel mechanisms of action to deliver effective control and eradication programs. Parasite resistance to all existing antimalarial classes, including the artemisinins, has been reported during their clinical use. A failure to generate new antimalarials with novel mechanisms of action that circumvent the current resistance challenges will contribute to a resurgence in the disease which would represent a global health emergency.

Author(s): 
Biagini, Giancarlo A.
Fisher, Nicholas
Shone, Alison E.
Mubaraki, Murad A.
Srivastava, Abhishek
Hill, Alisdair
Antoine, Thomas
Warman, Ashley J.
Davies, Jill
Pidathala, Chandrakala
Amewu, Richard K.
Leung, Suet C.
Sharma, Raman
Gibbons, Peter
Hong, David W.
Pacorel, Bénédicte
Lawrenson, Alexandre S.
Charoensutthivarakul, Sitthivut
Taylor, Lee
Berger, Olivier
Mbekeani, Alison
Stocks, Paul A.
Nixon, Gemma L.
Chadwick, James
Hemingway, Janet
Delves, Michael J.
Sinden, Robert E.
Zeeman, Anne-Marie
Kocken, Clemens H. M.
Berry, Neil G.
O'Neill, Paul M.
Ward, Stephen A.
Publication Title: 
Brain Research

Parkinson's disease (PD) is a movement disorder caused by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to nigrostriatal degeneration. The inhibition of mitochondrial respiratory chain complex I and oxidative stress-induced damage have been implicated in the pathogenesis of PD. The present study used these specific mitochondrial complex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP(+)) on striatal and cortical neurons in culture.

Author(s): 
Ying, Rong
Liang, Huan Ling
Whelan, Harry T.
Eells, Janis T.
Wong-Riley, Margaret T. T.
Publication Title: 
American Journal of Physiology. Regulatory, Integrative and Comparative Physiology

Comparing biological processes in closely related species with divergent life spans is a powerful approach to study mechanisms of aging. The oxidative stress hypothesis of aging predicts that longer-lived species would have lower reactive oxygen species (ROS) generation and/or an increased antioxidant capacity, resulting in reduced oxidative damage with age than in shorter-lived species.

Author(s): 
Shi, Yun
Pulliam, Daniel A.
Liu, Yuhong
Hamilton, Ryan T.
Jernigan, Amanda L.
Bhattacharya, Arunabh
Sloane, Lauren B.
Qi, Wenbo
Chaudhuri, Asish
Buffenstein, Rochelle
Ungvari, Zoltan
Austad, Steven N.
Van Remmen, Holly
Publication Title: 
Aging Cell

This review focuses on some of the 'hot topics' that fall under the general heading 'mitochondria and aging'. For each selected topic, we highlight recent publications that have either addressed specific problems within the field or presented novel findings of interest regarding the links between mitochondria and aging.

Author(s): 
Lambert, Adrian J.
Brand, Martin D.
Publication Title: 
American Journal of Physiology. Cell Physiology

Caloric restriction (CR) without malnutrition has been shown to increase maximal life span and delay the rate of aging in a wide range of species. It has been proposed that reduction in energy expenditure and oxidative damage may explain the life-extending effect of CR. Sex-related differences also have been shown to influence longevity and energy expenditure in many mammalian species. The aim of the present study was to determine the sex-related differences in rat liver mitochondrial machinery, bioenergetics, and oxidative balance in response to short-term CR.

Author(s): 
Valle, A.
Guevara, R.
García-Palmer, F. J.
Roca, P.
Oliver, J.
Publication Title: 
Cell Metabolism

Caloric restriction (CR) mitigates many detrimental effects of aging and prolongs life span. CR has been suggested to increase mitochondrial biogenesis, thereby attenuating age-related declines in mitochondrial function, a concept that is challenged by recent studies. Here we show that lifelong CR in mice prevents age-related loss of mitochondrial oxidative capacity and efficiency, measured in isolated mitochondria and permeabilized muscle fibers. We find that these beneficial effects of CR occur without increasing mitochondrial abundance.

Author(s): 
Lanza, Ian R.
Zabielski, Piotrek
Klaus, Katherine A.
Morse, Dawn M.
Heppelmann, Carrie J.
Bergen, H. Robert
Dasari, Surendra
Walrand, Stephane
Short, Kevin R.
Johnson, Matthew L.
Robinson, Matthew M.
Schimke, Jill M.
Jakaitis, Daniel R.
Asmann, Yan W.
Sun, Zhifu
Nair, K. Sreekumaran
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