Gracilaria bursa-pastoris (Gmelin) Silva extract attenuates ultraviolet B radiation-induced oxidative stress in human keratinocytes.

The purpose of this study was to assess the protective effects of an ethanol extract derived from the red alga Gracilaria bursa-pastoris (Gmelin) Silva (GBE) on ultraviolet B (UVB)-irradiated human HaCaT keratinocytes. GBE exhibited scavenging activity against intracellular reactive oxygen species that were induced by either hydrogen peroxide or UVB radiation. In addition, both the superoxide anion and the hydroxyl radical were scavenged by GBE in cell-free systems. GBE absorbed light in the UVB range (280-320 nm) of the electromagnetic spectrum and lessened the extent of UVB-induced oxidative damage to cellular lipids, proteins, and DNA. Finally, GBE-treated keratinocytes showed a reduction in UVB-induced apoptosis, as exemplified by fewer apoptotic bodies. These results suggest that GBE exerts cytoprotective actions against UVB-stimulated oxidative stress by scavenging ROS and absorbing UVB rays, thereby attenuating injury to cellular constituents and preventing cell death.

Ganoderma lucidum extract protects DNA from strand breakage caused by hydroxyl radical and UV irradiation.

The fruit bodies of Ganoderma lucidum have been used for the prevention and treatment of various diseases in the Orient. Its antitumor and immune enhancing properties, along with no cytotoxicity, raise the possibility that it could be effective in preventing oxidative damage and resulting disease. Using agarose gel electrophoresis, we have evaluated the potential of Ganoderma lucidum extract as a radioprotector and antioxidant defense against oxygen radical-mediated damage. Although the evidence presented here is based on in vitro using isolated DNA, the results clearly demonstrate that the hot-water extract of Ganoderma lucidum shows good radioprotective ability, as well as protection against DNA damage induced by metal-catalyzed Fenton reactions and UV irradiation. We also found that the water-soluble polysaccharide isolated from the fruit body of Ganoderma lucidum was as effective as the hot-water extract in protecting against hydroxyl radical-induced DNA strand breaks, indicating that the polysaccharide compound is associated with the protective properties. Our data suggest that Ganoderma mushroom merits investigation as a potential preventive agent in humans.

Nucleotide-induced mucin release from primary hamster tracheal surface epithelial cells involves the P2u purinoceptor.

Mucin release by airway surface epithelial cells is regulated by extracellular adenosine triphosphate (ATP) via a P2 purinoceptor-mediated mechanism. The objective of the present experiment was to examine the possible involvement of uridine triphosphate (UTP) in this purinergic signal transduction pathway. Using primary hamster tracheal surface epithelial cells, ATP and UTP were compared in their abilities: 1) to displace ATP gamma S35-binding to intact cells; 2) to accumulate inositol phosphates; and 3) to stimulate mucin release. Finally, the presence of a P2u receptor message was examined. Our results showed that: 1) UTP was much less effective than ATP in displacing ATP gamma S35-binding (median inhibitory concentrations (IC50S) 240 vs 2.9 microM); 2) UTP was more potent than ATP in accumulating inositol phosphates (100 vs 43% increase at 2mM); 3) UTP was equipotent with ATP in stimulating mucin release; 4) Northern blot analysis of messenger ribonucleic acids (mRNAs) with a mouse P2u receptor complementary deoxyribonucleic acid (cDNA) probe revealed a single specific band (2.8 kb), partial sequencing of which showed a great homology with those of human or mouse P2u receptors. We conclude that, although both ATP and UTP are equipotent in stimulating mucin release, their binding kinetics to the cell surface are quite different, suggesting the presence of a common binding domain which may be responsible for the mucin release by these nucleotides. We suggest that the P2u purinoceptor is likely to be responsible for mucin release by these nucleotides, probably via activation of phospholipase C.