Intact Lemna gibba plants were illuminated by photoinhibitory light in air, in air minus O2, in air minus CO2, and in pure N2. In pure N2, the degree of photoinhibition increased 3-5-times compared with that in air. This high degree of photoinhibition is described as photodamage. Photodamage was found to constitute a syndrome, that is, it is due to inactivation of multiple sites. These sites include RC II component(s) from P680 to Q(A); the Q(B)-Site; and a component of PS I. In photodamage, the donor side of PS II and PS II excitation energy transfer remain unimpaired, but the size of the PS I antenna seems to decrease. Photodamage is distinguishable from photoinactivation. Photoinactivation occurred in air and could be attributed to inhibition of electron transport from Q(A)- to Q(B). During photoinactivation the D1 protein of RC II became degraded faster than the detectable inhibition of Q(B) reduction. The photoinhibition-induced rise in F0 occurred only during the process of photodamage but not during that of photoinactivation, and was a secondary event which arose as a consequence of photodamage. Atmospheric O2 alleviated photodamage but increased photoinactivation. The light-induced Dl degradation and inhibition of Q(A) to Q(B) electron transfer were enhanced in vivo not only by O2 but also by depletion of CO2.