Cadmium　(Cd)　can　cause　cell　oxidative　stress　and　cytotoxicity.　Few　studies　have　focused　on　inhibitory　effects　on　Cd2+-induced　oxidative　stress　and　related　cytotoxicity.　Scanning　electrochemical　microscopy　(SECM)　is　a　highly　sensitive　and　non-invasive　electrochemical　analytical　method.　However,　no　information　exists　on　inhibitory　effects　on　Cd2+-induced　cell　oxidative　stress　using　SECM　technology.　Herein,　we　studied　the　effects　of　ascorbic　acid　(AsA),　zinc　chloride　(ZnCl2),　and　calcium　chelator　1,2-bis　(2-aminophenoxy)　ethane-N,N,N　＇,N　＇-tetraacetic　acid　tetraethoxy　methyl　ester　(BAPTA-AM)　on　cell　oxidative　stress　with　SECM.　Subsequently,　we　studied　the　inhibitory　effects　of　AsA,　ZnCl2,　and　BAPTA-AM　on　Cd2+-induced　cell　oxidative　stress.　Consequently,　50　mu　mol　L-1　AsA,　5　mu　mol　L-1　ZnCl2,　and　5　mu　mol　L-1　BAPTA-AM　did　not　produce　reactive　oxygen　species　(ROS)　and　had　little　effect　on　cell　viability.　However,　they　could　significantly　reduce　Cd2+-induced　excessive　ROS　and　alleviate　apoptosis　(P　＜　0.01).　Additionally,　AsA　had　the　strongest　inhibitory　effects　on　Cd2+-induced　oxidative　stress,　followed　by　BAPTA-AM　and　ZnCl2.　The　inhibitory　effects　of　AsA,　ZnCl2,　and　BAPTA-AM　on　Cd2+-induced　cytotoxicity　might　result　from　directly　scavenging　ROS　and　inhibiting　oxidative　stress-mediated　signal　transduction,　enhancing　antioxidant　activities　and　maintaining　cell　membrane　stabilities,　and　chelating　excess　calcium(2+)　(Ca2+)　to　hinder　its　subsequent　signal　transduction,　respectively.　Scavenging　excessive　ROS　and　inhibiting　cellular　oxidative　stress-mediated　signal　transduction　might　be　the　most　effective　way　to　alleviate　Cd2+-induced　cytotoxicity.　Our　study　provides　empirical　evidence　on　the　inhibitory　effects　of　AsA,　ZnCl2,　and　BAPTA-AM　as　specialized　inhibitors　against　Cd2+-induced　cellular　oxidative　stress　and　cytotoxicity,　providing　precious　ideas　for　detoxifying　toxic　environmental　metal　pollutants.