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.
