Oxygen is toxic to aerobic animals because it is univalently reduced inside cells to oxygen free radicals. Studies dealing with the relationship between oxidative stress and aging in different vertebrate species and in caloric-restricted rodents are discussed in this review. Healthy tissues mainly produce reactive oxygen species (ROS) at mitochondria. These ROS can damage cellular lipids, proteins and, most importantly, DNA. Although antioxidants help to control this oxidative stress in cells in general, they do not decrease the rate of aging, because their concentrations are lower in long- than in short-lived animals and because increasing antioxidant levels does not increase vertebrate maximum longevity. However, long-lived homeothermic vertebrates consistently have lower rates of mitochondrial ROS production and lower levels of steady-state oxidative damage in their mitochondrial DNA than short-lived ones. Caloric-restricted rodents also show lower levels of these two key parameters than controls fed ad libitum. The decrease in mitochondrial ROS generation of the restricted animals has been recently localized at complex I and the mechanism involved is related to the degree of electronic reduction of the complex I ROS generator. Strikingly, the same site and mechanism have been found when comparing a long- with a short-lived animal species. It is suggested that a low rate of mitochondrial ROS generation extends lifespan both in long-lived and in caloric-restricted animals by determining the rate of oxidative attack and accumulation of somatic mutations in mitochondrial DNA.

In this study, a simple time-lapse video recording system was used tocompare developmental kinetics of female and male bovine embryos producedin vitro. Following embryo sex determination, the timing of each cleavageup to the 4-cell stage was compared between the sexes from the videotapesafter culture in the presence and absence of glucose. In the secondexperiment, the consequences of exposure to a time-lapse video recording(TL) environment were studied by culturing embryos further until day 7in an incubator, followed by collection and sex determination of morulaeand blastocysts. In the absence of glucose, female embryos cleaved earlierthan male ones. In the presence of glucose, however, male embryos cleavedearlier than female ones. There was no difference in the number ofmorulae/blastocysts in the absence of glucose, but in the presence ofglucose more male than female embryos reached the morula and blastocyststage. Exposure to the TL environment itself also had a sex-relatedeffect, being more detrimental to male than female embryos. The differencein the number of functional X chromosomes between the sexes during earlypreimplantation development could explain these findings. In females, anincreased capacity for oxygen radical detoxification through the pentosephosphate pathway could result in a reduced cleavage rate. Furthermore,glucose may influence the expression of enzymes located on the Xchromosome. According to these results, a simple time-lapse videorecording system is suitable for investigating embryo developmentalkinetics and perhaps for the selection of embryos with the greatestdevelopmental potential.

Following hints from X-ray data (Ostermeier C et al., 1997, Proc Natl Acad Sci USA 94:10547–10553; Yoshikawa S et al., 1998, Science 280:1723–1729), chemical evidence is presented from four distantly related cytochrome-c oxidases for the existence of a copperB-coordinated His240–Tyr244) cross-link at the O2-activating Heme Fea3–CuB center in the catalytic subunit I of the enzyme. The early evolutionary invention of this unusual structure may have prevented demaging [bull]OH-radical release at e−-transfer to dioxygen and thus have enabled O2 respiration.