Milton, A.Zalewski, P.Ratnaike, R.2006-06-262006-06-262004BioMetals, 2004; 17(6):707-7130966-08441572-8773http://hdl.handle.net/2440/9824The original publication is available at www.springerlink.comAcute and chronic arsenic exposure results in toxicity in humans and causes many neurological and other manifestations. For the first time the present study reports that zinc decreases arsenic-induced apoptosis and also confirms a single report of apoptosis induced by arsenic in a neuronal cell line. Apoptosis measured by DEVD-caspase activity peaked between 10 M and 20 M of arsenic trioxide. Higher concentrations of arsenic up to 40 M caused increasing cell death with diminishing DEVD-caspase activity. The beneficial effect of zinc was proportional to its concentration with a significant decrease in arsenic-induced DEVD-caspase activity at 50 M and 75 M zinc (P<0.05). This finding may be of therapeutic benefit in people suffering from chronic exposure to arsenic from natural sources, a global problem especially relevant to millions of people on the Indian subcontinent.enNeuronsCell LineAnimalsMiceArsenicalsOxidesZincZinc SulfateSodium OxybateCaspasesEnzyme InhibitorsApoptosisEnzyme ActivationDose-Response Relationship, DrugPhenotypeTime FactorsArsenic TrioxideZinc protects against arsenic induced apoptosis in a neuronal cell line, measured by DEVD-caspase activityJournal article002004139510.1007/s10534-004-1210-30002265520000122-s2.0-1844436903456327Zalewski, P. [0000-0001-5196-2611]