Oxidative Stress in the Developing Rat Brain due to Production of Reactive Oxygen and Nitrogen Species.

Oxidative stress after birth led us to localize reactive oxygen and nitrogen species (RONS) production in the developing rat brain. Brains were assessed a day prenatally and on postnatal days 1, 2, 4, 8, 14, 30, and 60. Oxidation of dihydroethidium detected superoxide; 6-carboxy-2',7'-dichlorodihydrofluorescein diacetate revealed hydrogen peroxide; immunohistochemical proof of nitrotyrosine and carboxyethyllysine detected peroxynitrite formation and lipid peroxidation, respectively.

Lipophilic fluorescent products of free radicals.

Background: Fluorescent pigments are the end-products of reactions involving free radical attack on biological molecules and can be formed, for example, in reactions between lipid peroxidation products, mainly unsaturated aldehydes, with free amino groups. Their characteristic emission maximum was found to be at 420-470 nm after being excited at 340-390 nm. The mechanism of their formation and chemical identity has been revealed in many in vitro studies, in which reactive aldehydes were incubated with amino group-containing molecules.

Generation of hydrogen peroxide in the developing rat heart: the role of elastin metabolism.

Reports describing production of reactive oxygen species in neonatal heart are missing. As lysyl oxidase is potentially important source of H(2)O(2), we studied its role during ontogenic development of rat heart. H(2)O(2) was detected in thin sections of developing rat heart by fluorescence microscopy with the use of fluorescence probe 2'-7'-dichlorofluorescin.

Early postnatal development of rat brain is accompanied by generation of lipofuscin-like pigments.

The increased generation of free radicals results in the formation of fluorescent end-products of lipid peroxidation, lipofuscin-like pigments (LFPs). The authors observed that LFPs are generated in rat brain after a normal birth during 5 postnatal days. The experimental design of the study comprised 10 groups of animals.

Evaluation of lipofuscin-like pigments as an index of lead-induced oxidative damage in the brain.

This study was carried out to investigate the role of lead in the development of oxidative stress in the brain. We examined the rate of lipid peroxidation and we determined lipid fluorescence products (lipofuscin-like pigments - LFP) as a marker of lipid peroxidation after short in vitro incubation of rat brain homogenates with lead acetate (10(-2), 10(-4), 10(-6) M lead acetate, 2 h). Simultaneously we examined by the same method in vivo indices of oxidative stress in brains of mice exposed for 12 weeks to 0.

Evaluation of different methods detecting intracellular generation of free radicals.

Reactive oxygen species (ROS) play several biological roles. We investigated the applicability of fluorescent probes for their detection (i) in rabbit lens epithelial cells during ageing in culture, and (ii) in thin sections of rat heart. We used dihydroethidium (DHE), dichlorofluorescin (DCFH), and dihydrorhodamine 123 (DHR) together with detection of autofluorescence both in cells and in chloroform extracts.

Hypercapnia protects erythrocytes against free radical damage induced by hypoxia in exposed rats.

Several studies report that hypoxic exposure induces free radical oxidative damage in various tissues. The mechanism of this damage includes membrane lipid peroxidation which can be easily detected by measuring fluorescent end-products of the process, i.e.

Selenium protects the immature rat heart against ischemia/reperfusion injury.

The aim of the study was to find out whether administration of selenium (Se) will protect the immature heart against ischemia/reperfusion.The control pregnant rats were fed laboratory diet (0.237 mg Se/kg diet); experimental rats received 2 ppm Na(2)SeO(3) in the drinking water from the first day of pregnancy until day 10 post partum.

The effects of reactive oxygen and nitrogen species during yeast replicative ageing.

Free radicals are considered the most important cause of cellular ageing. We have investigated ageing process in the yeast Saccharomyces cerevisiae. We have compared the wild type strain with the mutant cells with constitutively active Ras oncogen, which generates increased amounts of free radicals.

Role of oxidative stress in PKC-delta upregulation and cardioprotection induced by chronic intermittent hypoxia.

The aim was to determine whether increased oxidative stress during the adaptation to chronic intermittent hypoxia (CIH) plays a role in the induction of improved cardiac ischemic tolerance. Adult male Wistar rats were exposed to CIH in a hypobaric chamber (7,000 m, 8 h/day, 5 days/wk, 24-30 exposures). Half of the animals received antioxidant N-acetylcysteine (NAC; 100 mg/kg) daily before the exposure; the remaining rats received saline.

Glycerophosphate-dependent hydrogen peroxide production by brown adipose tissue mitochondria and its activation by ferricyanide.

Oxidation of glycerophosphate (GP) by brown adipose tissue mitochondria in the presence of antimycin A was found to be accompanied by significant production of hydrogen peroxide. GP-dependent hydrogen peroxide production could be detected by p-hydroxyphenylacetate fluorescence changes or as an antimycin A-insensitive oxygen consumption. One-electron acceptor, potassium ferricyanide, highly stimulated the rate of GP-dependent antimycin A-insensitive oxygen uptake, which was prevented by inhibitors of mitochondrial GP dehydrogenase (mGPDH) or by coenzyme Q (CoQ).

Ultraviolet light-irradiated collagen III modulates expression of cytoskeletal and surface adhesion molecules in rat aortic smooth muscle cells in vitro.

Systemic and pulmonary hypertension is characterised by structural reconstruction of the vascular wall which includes hypertrophy and hyperplasia of vascular smooth muscle cells (VSMCs) and fibroproduction. We hypothesise that these changes are stimulated by non-enzymatic modification of collagen molecules in the injured vascular wall by radicals. We exposed collagen III to ultraviolet (UV) light irradiation which, as indicated by fluorescence and electrophoretic analyses, resulted in its fragmentation.