Copper and photosystem II: A controversial relationship

Abstract

Gorge. J. 1995. Copper and photosystem 11: A controversial relationship. -Pbysiol. Plant. 94: 174-180. Copper is an essential micronutrient for higher plants and algae and has a direct impact on photosynthesis. It is a constituent of the primary electron donor in photosystem 1. the Cu-protein plastocyanin. Many authors have also described Cu as a constituent of photosystem 11 (PSII). However, high Cu concentrations inhibit the photosynthetic electron transport, especially in PSII. In addition, both Cu deficiency and Cu toxicity interfere with pigment and lipid biosynthesis and, consequently, with chloroplast ultrastructure thus negatively influencing the photosynthetic efficiency. In this review, the different functions proposed for the metal in PSII are reviewed. Wilh reference to the effect of toxic Cu on PSII, the polemic results concerning its mechanism of action and Cu-hinding sites are discussed. Other effects of Cu loxicity and Cu deprivation on the thylakoid membrane are also briefly described.

Arrest of mitochondrial biogenesis in copper‐treated sycamore cells

“…At the level of whole plants, excess copper is known to inhibit growth and photosynthesis, the thresholds of toxicity being dependent on the plant species. The effects of copper on photosynthetic electron transport and photosystems have been extensively characterized using thylacoids or photosystem particles (for review, see [2,3]). Excess copper is also known (1) to inhibit a large number of enzymes, notably enzymes involved in the Benson-Clavin cycle, chlorophyll synthesis, and fatty acid metabolism, (2) to trigger oxidative damage and alteration of cell membrane properties, and (3) to induce thiol-rich polypeptides and enzymes, mostly peroxidases and esterases (for reviews, see [4][5][6][7]).…”

Influence of Cellular Density on Determination of EC50 in Microalgal Growth Inhibition Tests

“…The primary producers in seawater are microalgae, and heavy metals a!ect these organisms by enzyme inactivation, cellular transport interference, and/or interference with major nutrient assimilation (Price and Morel, 1994). Copper is especially toxic to aquatic biota (Sadiq, 1992), mainly phytoplankton (Riisgard et al, 1980;BaroH n et al, 1995). Recently, some authors presented evidence of the biomagni"cation processes for copper in trophic chains (Edding and Tala, 1996).…”

Genomic island genes in a coastal marine Synechococcus strain confer enhanced tolerance to copper and oxidative stress

“…Indeed, copper has been suggested to affect marine picocyanobacterial distribution (Mann et al, 2002), and marine Synechococcus strains have been shown to produce strong extracellular binding ligands in response to excess copper (Moffett and Brand, 1996). Copper toxicity is thought to result from a number of different mechanisms including the production of hydroxyl radicals, the blocking of essential metal binding sites and inhibition of electron transport in photosystem II (Baron et al, 1995;Sunda and Huntsman, 1998;Pinto et al, 2003). Much of the characterized copper stress response can consequently overlap with the oxidative stress response.…”