Is the blood donated by habitual nut quid chewers suitable for use in transfusion?

BACKGROUND/PURPOSE: Betel quid (BQ) chewing is a popular oral masticatory activity, and there are approximately 600 million BQ chewers worldwide. Although chewing BQ has been linked to the patho-genesis of oral cancer, leukoplakia, and oral submucous fibrosis. The question whether the mixed constituents present in areca nut, which may exert cytotoxic effects on red blood cells (RBCs), has never been addressed. METHODS: Heparinized blood specimens were obtained with informed consent from healthy laboratory personnel. RBCs were separated with the standard procedure and adjusted to 10% hematocrit with PBS. Various concentrations of areca nut extract (ANE; 100-800 microg/mL) were added to these RBC preparations and incubated at 37 degrees C for 4 hours. Two portions (0.4 mL each) of the incubated RBCs were then used for measuring osmotic deformability index and for observing RBC morphology with scanning electron microscopy. The remaining RBCs were used for determining membrane sulfhydryl groups and protein profiles by sodium dodecyl sulfate polyacrylamide gel electrophoresis. RESULTS: Blood incubated with various concentrations of ANE showed concentration-dependent decreases in osmotic deformability index and membrane sulfhydryl groups. Membrane protein profiles revealed a significant loss of the band 3 fraction, with the concomitant appearance of several new protein bands in the electropheretogram. Finally, drastic morphological changes of ANE-treated RBCs were observed. CONCLUSION: We suggest that to assure the quality of transfusion, the blood donated by a habitual BQ chewer should be used with caution because of its possible contamination with areca nut ingredients that may be cytotoxic to RBCs.

Dual effects of antioxidants in neurodegeneration: direct neuroprotection against oxidative stress and indirect protection via suppression of glia-mediated inflammation.

Oxidative stress, in which production of highly reactive oxygen species (ROS) and reactive nitrogen species (RNS) overwhelms antioxidant defenses, is a feature of many neurological diseases and neurodegeneration. ROS and RNS generated extracellularly and intracellularly by various processes initiate and promote neurodegeneration in CNS. ROS and RNS can directly oxidize and damage macromolecules such as DNA, proteins, and lipids, culminating in neurodegeneration in the CNS. Neurons are most susceptible to direct oxidative injury by ROS and RNS. ROS and RNS can also indirectly contribute to tissue damage by activating a number of cellular pathways resulting in the expression of stress-sensitive genes and proteins to cause oxidative injury. Moreover, oxidative stress also activates mechanisms that result in a glia-mediated inflammation that also causes secondary neuronal damage. Associated with neuronal injuries caused by many CNS insults is an activation of glial cells (particularly astrocytes and microglia) at the sites of injury. Activated glial cells are thus histopathological hallmarks of neurodegenerative diseases. Even though direct contact of activated glia with neurons per se may not necessarily be toxic, the immune mediators (e.g. nitric oxide and reactive oxygen species, pro-inflammatory cytokines and chemokines) released by activated glial cells are currently considered to be candidate neurotoxins. Therefore, study of the protective role of antioxidant compounds on inhibition of the inflammatory response and correcting the fundamental oxidant/antioxidant imbalance in patients suffering from neurodegenerative diseases are important vistas for further research. The purpose of this review is to summarize the current evidence in support of this critical role played by oxidative stress of neuronal and glial origin in neurodegenerative diseases. The mechanistic basis of the neuroprotective activity of antioxidants does not only rely on the general free radical trapping or antioxidant activity per se in neurons, but also the suppression of genes induced by pro-inflammatory cytokines and other mediators released by glial cells. We propose that combinations of agents which act at sequential steps in the neurodegenerative process can produce additive neuroprotective effects. A cocktail of multiple antioxidants with anti-inflammatory agents may be more beneficial in the prevention of neurodegenerative disease. A clearer appreciation of the potential therapeutic utility of antioxidants would emerge only when the complexity of their effects on mechanisms that interact to determine the extent of oxidative damage in vivo are more fully defined and understood.