Is Photoinhibition of Photosynthesis a Phototoxicity Mechanism

Photoinhibition of PS II, or simply photoinhibition, is a reaction in which visible light induces the loss of the electron transfer activity of PS II (Aro et al., 1993). The photodamage is a simple first-order process both in vitro (Jones and Kok, 1966) and in vivo (Tyystjärvi and Aro, 1996). Continuous repair of the photodamage explains why plants do not suffer from photoinhibitory symptoms under their normal growth light intensities.

The role of ROS in photoinhibition is poorly understood. Photoinhibition leads to an increase in the 1O2 content of leaves (Hideg et al., 1998), and 1O2 is involved in various hypothetical mechanisms of photoinhibition (Jung and Kim, 1990; Vass et al., 1992; Hideg et al, 1994; Keren et al, 1997; Santabarbara et al, 2001). The high sensitivity of PS II to XO2 generated from the outside (Knox and Dodge, 1985b) is compatible with the suggestions (Kim et al., 1993; Chung and Jung, 1995; Santabarbara et al., 2001) that photoinhibition is a Type II reaction in which the sensitizer may not be a functional part of PS II. However, photoinhibition occurs rapidly under anaerobic conditions (Hundal et al., 1990; Trebst and Depka, 1990), indicating that ROS play a secondary role. The partial reversibility of anaerobic photoinhibition prompted Vass et al. (1992) to suggest that XO2 is involved in an irreversible step of aerobic photoinhibition. The photooxidative damage caused by herbicides like DCMU (Pallett and Dodge, 1980) that block PS II electron transport but do not enhance formation of chlorophyll triplet by the "acceptor-side" mechanism of Vass et al. (1992) may suggest that light-induced 1O2 production is a general consequence of any block in PS II electron transport.

The action spectra of photoinhibition and D1 protein degradation show a high efficiency of ultraviolet-C to violet, and a low-efficiency visible tail with shallow peaks in red and possibly in green (Jones and Kok, 1966; Jung and Kim, 1990; Renger et al., 1989; Greenberg et al., 1989). Interpretation of the action spectrumhas been difficult, and virtually every peak has been explained with a separate photosensitizer, including chlorophyll, semiquinone, tyrosine, iron-sulfur centers, cytochromes and manganese (Jones and Kok, 1966; Jung and Kim, 1990; Greenberg et al., 1989; Renger et al., 1989; Santabarbara et al, 2001). The quantum yield of photoinhibition is independent of light intensity (Jones and Kok, 1966; Tyystjarvi and Aro, 1996), and the rate of photoinhibition can be lowered neither by reducing the size of the light-harvesting antenna of PS II nor by quenching of PS II excitations by artificial quenchers (Tyystjarvi et al., 1994, 1999). These data suggest that PS II antenna chlorophylls do not sensitize PS II to photoinhibition. The similarity of the action spectrum of photoinhibition (Jones and Kok, 1966) with the absorption spectrum of manganese gluconates (Bodini et al., 1976) led us to suggest that inactivation of the oxygen-evolving complex due to light absorption by manganese ions of the oxygen-evolving complex triggers photoinhibition not only in ultraviolet but also under visible light (Tyystjarvi et al., 2001).

Also PS I is light-sensitive to some extent (Sonoike, 1996). The susceptibility of PS I to photodamage depends strongly on temperature and plant species, and the inhibition saturates at moderate light intensity. Active oxygen produced by the PS I electron transfer chain is apparently involved in the reaction mechanism.

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