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Not AvailableHigh-temperature stress induces cellular changes leading to over-production of highly reactive oxygen species (ROS) which damage macromolecules and cell organelles, eventually resulting in cell death. Antioxidative metabolism in plants comprising of enzymatic and non-enzymatic antioxidants imparts tolerance by scavenging or detoxification of excess ROS. We investigated the response of major H2O2-detoxifying system, the AsA–GSH cycle in four genotypes of maize differing in heat sensitivity. Stress was imposed by staggered sowing so that one set of plants faced high-temperature stress at their anthesis-silking stage. The concentrations of H2O2 increased across the genotypes by high temperature; however, the increase was lesser in tolerant genotypes: NSJ 189 and NSJ 221. High-temperature stress led to an increase in the level of GSH and GSSG in all the genotypes, whereas GSH/GSSG decreased in sensitive genotypes: PSRJ 13099 and RJR 270. The glutathione S-transferase activity increased significantly under heat stress. APX, MDHAR and DHAR activities decreased under heat stress in the sensitive group. Under high temperature, GR activity remained unchanged in sensitive genotypes, while it increased significantly in tolerant genotypes. Ascorbate levels increased in tolerant genotypes, while a decline was observed in sensitive genotypes. Isoforms of APX showed some new bands in tolerant genotypes as well as higher intensity of the existing ones as compared to sensitive genotypes under stress conditions. Isoforms of GR did not show any genotypic differences under heat stress. Findings emphasized the importance and complexity of the AsA–GSH system in fine-tuning the redox metabolism under heat stress in maize. The study also suggested that the antioxidative enzymes of AsA–GSH cycle play a key role in sustaining the ROS homeostasis in cells, thus minimizing the potential toxic effects of ROS.Not Availabl