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Plant mitochondria differ from their mammalian counterparts in many respects, which are due to the unique and variable surroundings of plant mitochondria. In green leaves, plant mitochondria are surrounded by ample respiratory substrates and abundant molecular oxygen, both resulting from active photosynthesis, while in roots and bulky rhizomes and fruit carbohydrates may be plenty, whereas oxygen levels are falling. Several enzymatic complexes in mitochondrial electron transport chain (ETC) are capable of reactive oxygen species (ROS) formation under physiological and pathological conditions. Inherently connected parameters such as the redox state of electron carriers in the ETC, ATP synthase activity and inner mitochondrial membrane potential, when affected by external stimuli, can give rise to ROS formation via complexes I and III, and by reverse electron transport (RET) from complex II. Superoxide radicals produced are quickly scavenged by superoxide dismutase (MnSOD), and the resulting H(2)O(2) is detoxified by peroxiredoxin-thioredoxin system or by the enzymes of ascorbate-glutathione cycle, found in the mitochondrial matrix. Arginine-dependent nitric oxide (NO)-releasing activity of enzymatic origin has been detected in plant mitochondria. The molecular identity of the enzyme is not clear but the involvement of mitochondria-localized enzymes responsible for arginine catabolism, arginase and ornithine aminotransferase has been shown in the regulation of NO efflux. Besides direct control by antioxidants, mitochondrial ROS production is tightly controlled by multiple redundant systems affecting inner membrane potential: NAD(P)H-dependent dehydrogenases, alternative oxidase (AOX), uncoupling proteins, ATP-sensitive K(+) channel and a number of matrix and intermembrane enzymes capable of direct electron donation to ETC. NO removal, on the other hand, takes place either by reactions with molecular oxygen or superoxide resulting in peroxynitrite, nitrite or nitrate ions or through interaction with non-symbiotic hemoglobins or glutathione. Mitochondrial ROS and NO production is tightly controlled by multiple redundant systems providing the regulatory mechanism for redox homeostasis and specific ROS/NO signaling.

Numerous investigations link oxidative damage with differ-ent environmental and biotic stresses, such as heavy metalstress (Howlett and Avery 1997), ice encasement (Hethering-ton et al. 1987), senescence (Gidrol et al. 1989), salt stress(Guetadahan et al. 1997), anoxia (Chirkova et al. 1998), andthe hypersensitive response (Goodman 1994). Oxidativedamage can be detected by lipid peroxidation (LP), which isa natural metabolic process under normal conditions. It canbe divided into three stages: initiation, propagation, andtermination (Schiach 1992, Shewfelt and Purvis 1995). Theinitiation phase includes generation of reactive oxygen spe-cies (ROS) such as the superoxide anion, hydrogen peroxide,singlet oxygen, or the hydroxyl radical. ROS are byproductsof electron transport in chloroplasts, mitochondria, andplasma membranes (Elstner 1987). The imposition of stressresults in the elevation of ROS levels (Foyer et al. 1994,Alscher et al. 1997) and successively leads to lipid peroxida-tion and degradation. Polyunsaturated fatty acids (PUFA,the main components of membrane lipids) are susceptible toperoxidation as substrates. Hydroxyl radicals and singletoxygen can react with the methylene groups of PUFAforming conjugated dienes, lipid peroxy radicals, and hy-droperoxides (Smirnoff 1995). The peroxy radicals can in-volve new molecules of PUFA in the process thus initiatingthe propagation phase (Frankel 1985).For each stage of this free radical chain reaction, plantcells have a defense system eliminating ROS and toxicproducts of LP (Buettner 1993, Smirnoff 1995). Undersevere stress conditions, elevated levels of free radicals canbreak down the defense mechanisms of the cell.However, until now it is not quite clear whether peroxida-tion can be considered a cause of membrane damage andmetabolic disorders, or a secondary effect of these processes.This problem arises from controversial observations con-cerning the mechanisms and products of LP in plant tissues.Recently, a new comprehensive model for lipid peroxidationin plant tissues has been developed (Shewfelt and Purvis1995). This model emphasizes the importance of chemicalrather than biochemical processes in the oxidative stress.Free radicals are regarded as a common link between many