Oxidative stress results from a disruption of the prooxidant/antioxidant cellular balance and monitoring free radical status becomes an interesting challenge in animal and human nutrition. In the present work, merits and limitations of different analytical techniques (HPLC, GC-MS, fluorometric and colourometric assays, ELISA, gel electrophoresis) for the measurement of radical mediated alterations in the cellular integrity of lipids (malondialdehyde, hydrocarbon gases, F2-isoprostanes) proteins (protein carbonyls, 3-nitrotyrosine) and DNA (8-hydroxy-2'-deoxyguanosine) are discussed. Besides these indirect methods, owing to the fact that free radicals are paramagnetic, electron paramagnetic resonance spectroscopy combined with spin trapping has become a valuable tool to directly assess and to better understand the mechanisms of free radical reactions. With this approach a radical that is too short-lived to be detected, adds to a spin-trapping agent to form a relatively long-lived radical adduct. Information obtained from the hyperfine splitting of the spin-trapped adduct can provide identification and quantification of the originally generated free radicals.
Oncornavirus‐like particles have been consistently observed over a period of 3 years in HeLa cells obtained from several laboratories. The particles mature by budding, in that previously fully assembled A‐type‐like particles are enveloped by the protruding cell membrane with subsequent release of the virion. When compared morphologically to B‐ and C‐type particles, distinct differences were observed; however, the HeLa particles closely resemble two primate viruses, namely the Mason‐Pfizer monkey virus and a recently discovered virus derived from human brain cells. HeLa particles demonstrate a narrow host range. Thus a new morphological group of viruses emerges that might be specific for primates.
The cytotoxicity of trivalent and pentavalent inorganic arsenic salts was determined in mouse fibroblasts in vitro. Concentrations of As (III) in the microM range led to a reduction of proliferation and viability with a concomitant increase in LDH release and stimulation of lactic acid production. Similar effects were noted with approximately 10-fold greater molar concentrations of As(V). Cells pretreated with a low As(III) concentration are less sensitive to toxic doses of As(III) or As(V). Uptake of As(III) by the fibroblasts is greater than that of As(V). Both forms of inorganic arsenic are converted intracellularly to monomethylarsonic (MMA) and dimethylarsinic (DMA) acids, which are then released into the culture medium. In As-pretreated cells, which are more resistant to As toxicity, biotransformation of inorganic arsenic to MMA and DMA is increased.
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