Search Results

You are looking at 91 - 100 of 344 items for :

  • reactive oxygen species x
  • All content x
Clear All
Free access

T C Alba-Loureiro, S M Hirabara, J R Mendonça, R Curi, and T C Pithon-Curi

et al. 1974 ), phagocytosis ( Nolan et al. 1978 ) and production of reactive oxygen species (ROS) ( Sagone et al. 1983 ). Neutrophil functions require energy ( Mowat & Baum 1971 , McMurray et al. 1990 , Walrand et al. 2004 ), which

Free access

Xiaochuan Chen, Amy C Kelly, Dustin T Yates, Antoni R Macko, Ronald M Lynch, and Sean W Limesand

and increases accumulation of reactive oxygen species in fetal sheep islets . Journal of Endocrinology 212 327 – 342 . ( doi:10.1530/JOE-11-0300 ) Greenough A Nicolaides KH Lagercrantz H 1990 Human fetal sympathoadrenal responsiveness

Free access

Lucy M Hinder, Anuradha Vivekanandan-Giri, Lisa L McLean, Subramaniam Pennathur, and Eva L Feldman

is decreased in sciatic nerve and DRG tissue in db/db mice Aconitase catalyzes the conversion of CIT to ICIT in the TCA cycle and is the most sensitive TCA cycle enzyme to reactive oxygen species (ROS) inhibition ( Tretter & Adam-Vizi 2000 ). Work by

Free access

Sehee Kim, Minho Moon, and Seungjoon Park

al . 1998 ). Since microglia are a principal source of a variety of cytotoxic compounds, including reactive oxygen species, reactive nitrogen species, pro-inflammatory cytokines, and prostaglandins ( Banati et al . 1993 ); microglial activation is

Free access

Pongpan Tanajak, Siriporn C Chattipakorn, and Nipon Chattipakorn

acetyl CoA dehydrogenase; mcpt1α, mitochondrial carnitine palmitoyltransferase 1; ISO, isoproterenol; LPS, lipopolysaccharide; ROS, reactive oxygen species; pfu, plaque-forming units; i.m., intramuscular; TNFα, TNFα tumor necrosis factor alpha; NCMs

Free access

Sujith Rajan, Kripa Shankar, Muheeb Beg, Salil Varshney, Abhishek Gupta, Ankita Srivastava, Durgesh Kumar, Raj K Mishra, Zakir Hussain, Jiaur R Gayen, and Anil N Gaikwad

, Kim et al . 2015 ). Hyperinsulinemia has been reported to cause mitochondrial dysfunction in white adipocytes, muscle, and heart through generation of reactive oxygen species, free radicals, and ER stress. Earlier Shabalina and coworkers have reported

Free access

Hao Wu, Junduo Wu, Shengzhu Zhou, Wenlin Huang, Ying Li, Huan Zhang, Junnan Wang, and Ye Jia

:1000). Quantitative analysis of reactive oxygen species (ROS) and lipid peroxides ROS and malondialdehyde (MDA) levels were measured in cell lysates, by using a ROS assay kit (Nanjing Jiancheng Bioengineering Institute, Nanjing, Jiangsu, PRC) and a lipid

Free access

Gonzalo Alba, Consuelo Santa-María, María Edith Reyes-Quiroz, Rajaa El Bekay, Isabel Geniz, José Martín-Nieto, Elizabeth Pintado, and Francisco Sobrino

Introduction Redox regulation of cellular processes is currently a focus of intense research ( Finkel 2011 ). The intracellular redox status is determined by the balance between reactive oxygen species (ROS) and the cellular antioxidant defenses

Free access

S Morimoto, C A Mendoza-Rodríguez, M Hiriart, M E Larrieta, P Vital, and M A Cerbón

) depletion, a mechanism well documented in rodent islets ( Yang & Wright 2002 ). During STZ metabolism, various toxic intermediates are produced, including methyl cations, methyl radicals, reactive oxygen species (ROS) and nitric oxide (NO) ( Peschke et al

Open access

Helen L Jeanes, Caroline Tabor, Darcey Black, Antwan Ederveen, and Gillian A Gray

Pedram A Razandi M Levin ER 2006 Estrogen prevents cardiomyocyte apoptosis through inhibition of reactive oxygen species and differential regulation of p38 kinase isoforms . Journal of Biological Chemistry 281 6760 – 6767 . Lesnefsky EJ Moghaddas