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Photoinhibition. Exposure of photosynthetic organisms to moderate or high intensity light
eventually results in a loss of electron transport capacity which has been broadly termed
photoinhibition (Neale, 1987). The intensity and duration of illumination required to produce
a given amount of photoinhibition varies between species and with the growth conditions to
which the organism is adapted. Photoinhibitory damage may be reversible or irreversible, the
latter generally requiring higher intensity/longer duration exposure. Under physiological
conditions, reversible photoinhibition is much more common. Damage appears to be localized
in the PS II reaction center complex, resulting in a loss of photochemical charge separation
(Kyle and Ohad, 1986). Recovery requires synthesis and insertion of new proteins into the
complex. A common characteristic for reversible photoinhibition of PS II is a loss of variable
fluorescence. Under a fixed set of measuring conditions, the extent of variable fluorescence
measured in the presence of DCMU declines in proportion to the fraction of PS II reaction
centers that are photoinhibited (Bjorkman and Demmig, 1987). The decrease in variable
fluorescence accompanying the loss of reaction center photochemistry suggests that
photoinhibition induces the formation of a new quenching reaction in PS II. A satisfactory
mechanism explaining these observations is not yet known. As would be expected,
photoinhibition also results in a decreased capacity for electron transport and quantum yield
of photochemistry in PS II (Bjorkman and Demmig, 1987). Fluorescence quenching due to
photoinhibitory damage (qJ occurs at both saturating and limiting light intensities in
approximately a dose dependent manner. Recovery from photoinhibition shows a similar
dependence, requiring tens of minutes to many hours.
Quenching related to changes in antenna size. The lifetime of an excitation in the PS II (and
PS I) antennae is determined by the efficiency of photochemistry in the reaction center and
by the size of the antenna (Owens et al., 1987; Holzwarth, 1987). The contribution of
antenna size can be understood as follows: it is known that an excited state is essentially
delocalized among the antenna pigments during its lifetime, spending no more time on the
reaction center than on any other pigment. Because fluorescence yield and excited state
lifetime are linearly related (equation 4), the fluorescence yield increases with increasing
antenna size because the lifetime of the excited state increases as it migrates over a larger
number of antenna pigments.
Photoinhibition. Exposure of photosynthetic organisms to moderate or high intensity light
eventually results in a loss of electron transport capacity which has been broadly termed
photoinhibition (Neale, 1987). The intensity and duration of illumination required to produce
a given amount of photoinhibition varies between species and with the growth conditions to
which the organism is adapted. Photoinhibitory damage may be reversible or irreversible, the
latter generally requiring higher intensity/longer duration exposure. Under physiological
conditions, reversible photoinhibition is much more common. Damage appears to be localized
in the PS II reaction center complex, resulting in a loss of photochemical charge separation
(Kyle and Ohad, 1986). Recovery requires synthesis and insertion of new proteins into the
complex. A common characteristic for reversible photoinhibition of PS II is a loss of variable
fluorescence. Under a fixed set of measuring conditions, the extent of variable fluorescence
measured in the presence of DCMU declines in proportion to the fraction of PS II reaction
centers that are photoinhibited (Bjorkman and Demmig, 1987). The decrease in variable
fluorescence accompanying the loss of reaction center photochemistry suggests that
photoinhibition induces the formation of a new quenching reaction in PS II. A satisfactory
mechanism explaining these observations is not yet known. As would be expected,
photoinhibition also results in a decreased capacity for electron transport and quantum yield
of photochemistry in PS II (Bjorkman and Demmig, 1987). Fluorescence quenching due to
photoinhibitory damage (qJ occurs at both saturating and limiting light intensities in
approximately a dose dependent manner. Recovery from photoinhibition shows a similar
dependence, requiring tens of minutes to many hours.
Quenching related to changes in antenna size. The lifetime of an excitation in the PS II (and
PS I) antennae is determined by the efficiency of photochemistry in the reaction center and
by the size of the antenna (Owens et al., 1987; Holzwarth, 1987). The contribution of
antenna size can be understood as follows: it is known that an excited state is essentially
delocalized among the antenna pigments during its lifetime, spending no more time on the
reaction center than on any other pigment. Because fluorescence yield and excited state
lifetime are linearly related (equation 4), the fluorescence yield increases with increasing
antenna size because the lifetime of the excited state increases as it migrates over a larger
number of antenna pigments.