Selenium restores mitochondrial dysfunction to reduce Cr-induced cell apoptosis in Chinese cabbage (Brassica campestris L. ssp. Pekinensis) root tips

Abstract

Chromium (Cr) disrupts the growth and physiology of plants. Selenium (Se) is considered as a promising option to help plants ameliorate Cr toxicity. To investigate the effects of exogenous Se on reactive oxygen species (ROS) burst and programmed cell death (PCD) in root tip cells under Cr stress, hydroponic experiments were carried out with Chinese cabbage seedlings grown in Hoagland solution containing 1 mg L-1 Cr and 0.1 mg L-1 Se. Results showed that Se scavenged the overproduction of H2O2 and O2－·, and alleviated the level of lipid peroxidation in root tips stressed by Cr. Moreover, Se effectively prevented DNA degradation and reduced the number of apoptotic cells in root tips. Compared with Cr treatment, Se supplementation reduced the content of ROS and malondialdehyde in mitochondria by 38.23% and 17.52%, respectively. Se application decreased the opening degree of mitochondrial permeability transition pores by 32.30%, increased mitochondrial membrane potential by 40.91%, alleviated the release of cyt c from mitochondria into cytosol by 18.42% and caused 57.40% decrease of caspase 3-like protease activity, and thus restored mitochondrial dysfunction caused by Cr stress. In addition, the alteration of Se on mitochondrial physiological properties maintained calcium homeostasis between mitochondria and cytosol, which further contributed to reducing the appearance of Cr-induced PCD. Findings suggested that Se restored mitochondrial dysfunction, which further rescued root tip cells from PCD, consequently activating defense strategies to protect plants from Cr toxicity and maintaining plant growth.