Clonal tissue of the marine chlorophyte macroalga, Ulva rotundata Blid., was transferred from 100 to 1700-mu-mol photons . m-2 . s-1 under limiting (1.5-mu-M NH4+ maximum, N/P = 2) and sufficient (15-mu-M NH4+ maximum, N/P = 20) nitrogen supply at 18-degrees-C and 11 h light-13 h darkness daily. Photoinhibition was assayed by light-response curves (photosynthetic O2 exchange), and chlorophyll fluorescence at 77 K and room temperature. Daily surface-area growth rate (mu-SA) in N-sufficient plants increased sixfold over 3 d and was sustained at that level. During this period, respiration (R(d)) doubled and light-saturated net photosynthesis capacity (P(m)) increased by nearly 50%, indicating acclimation to high light. Quantum yield (phi) decreased by 25% on the first day, but recovered completely within one week. The ratio of variable to maximum fluorescence (F(v)/F(m)) also decreased markedly on the first day, because of an increase in initial fluorescence (F(o)) and a decrease in F(m), and partially recovered over several days. Under the added stress of N deficiency, mu-SA accelerated fivefold over 4 d, despite chronic photoinhibition, then declined along with tissue-N. Respiration doubled, but P(m) decreased by 50% over one week, indicating inability to acclimate to high light. Both phi and F(v)/F(m) decreased markedly on the first day and did not significantly recover. Changes in F(o), F(m) and xanthophyll-cycle components indicate concurrent photodamage to photosystem II (PSII) and photo-protection by thermal deexcitation in the antenna pigments. Increasing mu-SA coincided with photoinhibition of PSII. Insufficient diel-carbon balance because of elevated R(d) and declining P(m) and tissue-N, rather than photo-chemical damage per se, was the apparent proximate cause of decelerating growth rate and subsequent tissue degeneration under N deficiency in U. rotundata.