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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Photoinhibition of photosystem II was studied in vivo with bean (Phaseolus vulgaris) plants grown in the presence of 0.3 (control), 4, or 15 microM Cu(2+). Although photoinhibition, measured in the presence of lincomycin to block concurrent recovery, is faster in leaves of Cu(2+)-treated plants than in control leaves, thylakoids isolated from Cu-treated plants did not show high sensitivity to photoinhibition. Direct effects of excess Cu(2+) on chloroplast metabolism are actually unlikely, because the Cu concentration of chloroplasts of Cu-treated plants was lower than that of their leaves. Excess Cu in the growth medium did not cause severe oxidative stress, collapse of antioxidative defenses, or loss of photoprotection. Thus, these hypothetical effects can be eliminated as causes for Cu-enhanced photoinhibition in intact leaves. However, Cu treatment lowered the leaf chlorophyll (Chl) concentration and reduced the thylakoid membrane network. The loss of Chl and sensitivity to photoinhibition could be overcome by adding excess Fe together with excess Cu to the growth medium. The addition of Fe lowered the Cu(2+) concentration of the leaves, suggesting that Cu outcompetes Fe in Fe uptake. We suggest that the reduction of leaf Chl concentration, caused by the Cu-induced iron deficiency, causes the high photosensitivity of photosystem II in Cu(2+)-treated plants. A causal relationship between the susceptibility to photoinhibition and the leaf optical density was established in several plant species. Plant species adapted to high-light habitats apparently benefit from thick leaves because the rate of photoinhibition is directly proportional to light intensity, but photosynthesis becomes saturated by moderate light.
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PMID:Excess copper predisposes photosystem II to photoinhibition in vivo by outcompeting iron and causing decrease in leaf chlorophyll. 1211 89

The effects of iron deficiency on cell culture growth, cell respiration, mitochondrial oxidative properties, and the electron transport chain were studied with suspension-cultured sycamore (Acer pseudoplatanus L.) cells. Iron deprivation considerably decreased the initial growth rates and limited the maximum density of the cells. Under these conditions, the cells remained swollen throughout their growth. The absence of iron led to a steady decline in the uncoupled rate of O2 consumption. When the uncoupled rate of O2 uptake closely approximated the respiratory rate, the cells began to collapse. At this stage, the level of all the cytochromes and electron paramagnetic resonance-detectable Fe-S clusters of the mitochondrial inner membrane were dramatically decreased. Nevertheless, it appeared from substrate oxidation measurements that this overall depletion in iron-containing components solely disturbed the functioning of complex II, whereas neither complexes I, III, or IV, nor the machinery involved in ATP synthesis, was apparently impaired in iron-deficient mitochondria. However, our results suggest that the impairment of complex II resulted in a strong reduction of the overall capacity of the mitochondrial electron transport chain, which was responsible for determining the rate of endogenous respiration in sycamore cells. Finally, this situation led to a depletion of various energy metabolites that could contribute to the premature cell death.
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PMID:Effect of Iron Deficiency on the Respiration of Sycamore (Acer pseudoplatanus L.) Cells. 1223 26

This paper examines three hypotheses constructed to explain the cause of the desferrioxamine/prochlorperazine coma. This deep and prolonged (2-3days) coma results when normal doses of two widely used therapeutic agents (the iron chelator desferrioxamine and the dopamine receptor blocker prochlorperazine) are administered together in normal doses in humans and rats. The coma is more severe in iron-deficient rats suggesting that removal of iron and resulting neuronal iron deficiency by desferrioxamine is a contributory cause. Iron and dopamine are linked in the O'Brien cycle in which redox cycling occurs between ferric and ferrous iron linked to cycling between a catecholamine and its o-quinone. This cycle is a powerful transmuter of superoxide, that converts five molecules of superoxide into two molecules of water and three molecules of hydrogen peroxide. Hydrogen peroxide is a vital ingredient in many redox signalling mechanisms in neurons. Dopamine D2 receptor antagonists also inhibit the activation of hydrogen peroxide-producing superoxide dismutase in the postsynaptic neuron. The coma might be therefore due to collapse of the O'Brien cycle and lack of SOD resulting in a fall in hydrogen peroxide levels. Three different microanatomical loci are evaluated to explain how the coma might result from these redox reactions.
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PMID:Does the O'Brien cycle occur in vivo as a key component in H(2)O(2) production and redox signalling? 2110 58