On 'Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria' by Julio F. Turrens, Adolfo Alexandre and Albert L. Lehninger.

This commentary addresses the article, "Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria," Arch. Biochem. Biophys.

Mitochondrial DNA damage triggers mitochondrial-superoxide generation and apoptosis.

Recently, it has become apparent that mitochondrial DNA (mtDNA) damage can rapidly initiate apoptosis independent of mutations, although the mechanism involved remains unclear. To elucidate this mechanism, angiotensin II-mediated apoptosis was studied in cells that were transduced with a lentiviral vector to overexpress the DNA repair enzyme 8-oxoguanine glycosylase or were treated with inhibitors known to block angiotensin II-induced mtDNA damage. Cells exhibiting angiotensin II-induced mtDNA damage showed two phases of superoxide generation, the first derived from NAD(P)H oxidase and the second of mitochondrial origin, whereas cells prevented from experiencing mtDNA damage importantly exhibited only the first phase.

A simple classroom teaching technique to help students understand Michaelis-Menten kinetics.

A new, simple classroom technique helps cell biology students understand principles of Michaelis-Menten enzyme kinetics. A student mimics the enzyme and the student's hand represents the enzyme's active site. The catalytic event is the transfer of marbles (substrate molecules) by hand from one plastic container to another.

Teaching research integrity and bioethics to science undergraduates.

Undergraduate students in the Department of Biomedical Sciences at the University of South Alabama, Mobile, are required to take a course entitled "Issues in Biomedical Sciences," designed to increase students' awareness about bioethical questions and issues concerning research integrity. This paper describes the main features of this course and summarizes the results of a survey designed to evaluate the students' perceptions about the course. A summary of this study was presented at the 2002 Conference on Research Integrity in Potomac, MD, sponsored by the Office of Research Integrity of the National Institutes of Health.

Oxidative stress and antioxidant defenses: a target for the treatment of diseases caused by parasitic protozoa.

Parasitic protozoa cause several diseases, affecting hundreds of millions, particularly in underdeveloped countries. Although these organisms are eukaryotic cells, some of them present major differences with their mammalian host in selected metabolic pathways. These differences may be exploited as targets for developing better pharmacological agents for the treatment of specific parasitic diseases.

Mitochondrial formation of reactive oxygen species.

The reduction of oxygen to water proceeds via one electron at a time. In the mitochondrial respiratory chain, Complex IV (cytochrome oxidase) retains all partially reduced intermediates until full reduction is achieved. Other redox centres in the electron transport chain, however, may leak electrons to oxygen, partially reducing this molecule to superoxide anion (O2-*).

Extramitochondrial localization of NADH-fumarate reductase in trypanosomatids.

Trypanosoma brucei procyclic trypomastigotes and T. cruzi epimastigotes (both Tulahuen and Y strains) were permeabilized by incubation with increasing amounts of digitonin, causing enzymes to be released from different intracellular compartments. After 10 min incubation with digitonin, the cells were centrifuged and the activity of marker enzymes (aspartate-dependent malic enzyme for cytoplasm, hexokinase for glycosomes and either isocitrate dehydrogenase or citrate synthase for mitochondria) was analyzed in the supernatant.

Oxidant species trigger late preconditioning against myocardial stunning in conscious rabbits.

Conscious rabbits underwent six 4-min occlusion and 4-min reperfusion cycles for 3 consecutive days (day 1, 2, and 3); on day 1, rabbits received intravenous vehicle [preconditioning (PC)] (group I, n = 6), superoxide dismutase (SOD; group II, n = 5), catalase (group III, n = 6), or the hydroxyl radical (. OH) and peroxynitrite (ONOO-)) scavenger N-2-mercaptopropionyl glycine (MPG [group IV], n = 6). In the PC group, the recovery of systolic wall thickening (WTh) after the sixth reperfusion was markedly improved on days 2 and 3 compared with day 1 and the total deficit of WTh was correspondingly reduced, indicating a late PC effect against myocardial stunning.