Abstract
A general status of oxidative stress in plants caused by exposure to elevated metal concentrations in the environment coincides with a constraint on mitochondrial electron transport, which enhances ROS accumulation at the mitochondrial level. As mitochondria are suggested to be involved in redox signaling under environmental stress conditions, mitochondrial ROS can initiate a signaling cascade mediating the overall stress response, i.e., damage versus adaptation. This review highlights our current understanding of metal-induced responses in plants, with focus on the production and detoxification of mitochondrial ROS. In addition, the potential involvement of retrograde signaling in these processes will be discussed.
Highlights
Worldwide, metal industry and agricultural use of metal-containing fertilizers and pesticides have contributed significantly to metal pollution
As mitochondria are key players in cellular redox homeostasis and signaling [16], this review focuses on reactive oxygen species (ROS) production and antioxidative defense mechanisms in mitochondria and how these processes are affected by metal exposure
Results of our work indicate a possible co-regulation of alternative oxidase (AOX) and alternative NAD(P)H dehydrogenases (NDs) transcription in Cd-exposed Arabidopsis roots and leaves [64]
Summary
Metal industry and agricultural use of metal-containing fertilizers and pesticides have contributed significantly to metal pollution. Resulting concentrations of toxic metals in the environment often exceed those from natural sources [1] Metals such as copper (Cu), iron (Fe), nickel (Ni) and zinc (Zn) are essential for functioning of physiological and biochemical processes and, for normal growth and development of organisms [2,3]. In addition to enzymatic pathways, excess metals increase ROS production in subcellular organelles such as peroxisomes, chloroplasts and mitochondria, which together constitute the predominant sources of ROS production in plants Their highly oxidizing nature and the presence of electron transport chains in chloroplasts and mitochondria makes both organelles a preferential site for metal-induced ROS production [11,14]. As mitochondria are key players in cellular redox homeostasis and signaling [16], this review focuses on ROS production and antioxidative defense mechanisms in mitochondria and how these processes are affected by metal exposure. The resulting oxidative challenge in mitochondria further implicates downstream signaling responses via ROS and/or other signaling intermediates, which will be discussed in the light of metal stress in this review
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