Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to obtain further information on the viability of organ-cultured human cornea. We thus used a specific staining method for succinate dehydrogenase (SDH), which is located in the membrane system of vital mitochondria. We examined fresh and long-term-cultured human corneas. After an initial incubation period in dextran-free culture medium, corneas were stored in a medium containing dextran. With respect to different appearances of the SDH staining, minimal essential medium without dextran seems to have a positive effect on the condition of epithelial cells. After renewal of the medium, keratocytes showed a brief improvement followed by a delayed deterioration, while the endothelial cells were severely damaged. However, best results for all three cell types were observed on the fourth day in a medium containing dextran. We therefore conclude that these corneas were best suited for transplantation.
Cornea 1995 Sep
PMID:Remarks on the vitality of the human cornea after organ culture. 853 64

Much attention has been focused on the hypothesis that oxidative damage plays a part in cellular and organismal aging. Oxygen is initially converted to superoxide anion (O2), one of the reactive oxygen species (ROS), by electrons mainly leaked from complex III in the electron transport system present in mitochondria, where it is the major endogenous source of ROS. We have shown that a mutation in a subunit, cytochrome b large subunit (SDHC), of complex II, also results in increasing O2 production and therefore leads to apoptosis and precocious aging in Caenorhabditis elegans. Recently, individuals with an inherited propensity for vascularized head and neck tumors (ie, paragangliomas) have been shown to possess one of several mutations in complex II. To further explore the role of oxidative stress from mitochondria on apoptosis and cancer, we established a transgenic cell line with a point mutation at the ubiquinone binding region in the SDHC gene. As expected, this mutation increased O2 production from complex II and led to excess apoptosis. Moreover, a significant fraction of the surviving cells from the apoptosis were transformed, as evidenced by increased tumor formation, after injection into mice. Oxidative stress results in damage to the cellular components including mitochondria and therefore leads to apoptosis. Furthermore, oxidative stress seems to cause mutations in DNA and leads to cancer. It is suggested that oxidative stress from mitochondria plays an important role in apoptosis, which leads to precocious aging and cancer.
Cornea 2007 Oct
PMID:Role of oxidative stress from mitochondria on aging and cancer. 1788 13