[3][4] However, when present in excess, ROS can cause damage to proteins, lipids and DNA by reacting with these biomolecules to modify or destroy their intended function.
As an example, the occurrence of ROS have been linked to the aging process in humans, as well as several other diseases including Alzheimer's, rheumatoid arthritis, Parkinson's, and some cancers.
[5] Their potential for damage also makes reactive oxygen species useful in direct protection from invading pathogens,[6] as a defense response to physical injury,[7][8][9][10] and as a mechanism for stopping the spread of bacteria and viruses by inducing programmed cell death.
[11] Reactive oxygen species are present in low concentrations in seawater and are produced primarily through the photolysis of organic and inorganic matter.
[12] However, the biological production of ROS, generated through algal photosynthesis and subsequently 'leaked' to the environment, can contribute significantly to concentrations in the water column.
[16][17] This ROS has the potential to harm nearby organisms,[18][19] and, in fact, has been implicated as the cause of massive fish, bacteria, and protist mortalities.
[24][25][26] The ROS most likely released to the environment are those produced at the cell surface as electrons get "leaked" from the respiratory chain and react with molecular oxygen, O2.
[30] According to Blough & Zepp,[30] superoxide is one of the hardest reactive oxygen species to quantify because it is present in low concentrations: 2×10−12 M in the open ocean and up to 2×10−10M in coastal areas.
As a charged radical species, superoxide is unlikely to significantly affect an organism's cellular function since it is not able to easily diffuse through the cell membrane.
[12][30] H2O2 is important in aquatic environments because it can oxidize dissolved organic matter and affect the redox chemistry of iron, copper, and manganese.
[33] Since hydrogen peroxide, as an uncharged molecule, diffuses easily across biological membranes it can directly damage cellular constituents (DNA and enzymes) by reacting with them and deactivating their functions.
Indirectly, the hydroxyl radical can result in significant biogeochemical changes in marine systems by influencing the cycling of dissolved organic matter and trace metal speciation.
Both intracellular and extracellular reactive oxygen species can be removed from the environment by antioxidants produced biologically as a defense mechanism.
In a comparison of 37 species of marine microalgae, including dinoflagellates, rhaphidophytes, and chlorophytes, Marshall et al.[17] also found a direct relationship between cell size and the amount of superoxide produced.
[50] Tang & Gobler[51] also found that cell density was inversely related to ROS production for the alga Cochlodinium polykrikoides.
[53] Since superoxide is produced through the auto-oxidation of an electron acceptor in photosystem I during photosynthesis, one would expect a positive relationship between light levels and algal ROS production.
Similarly, in Heterosigma akashiwo, the depletion of iron and an increase in temperature, not light intensity, resulted in enhanced production of ROS.
The active release of reactive oxygen species from cells has a variety of purposes, including a means to deter predators, or a chemical defense for the incapacitation of competitors.
[25] One of the most common mechanisms of cellular injury is the reaction of ROS with lipids, which can disrupt enzyme activity and ATP production, and lead to apoptosis.
[37] Reactions of ROS with proteins can modify amino acids, fragment peptide chains, alter electrical charges, and ultimately inactivate an enzyme's function.
[64][65] Reactive oxygen species are especially inexpensive to produce as defense chemicals, simply because they are not composed of metabolically costly elements such as carbon, nitrogen, or phosphate.
Reactive oxygen species produced by phytoplankton have been linked to deaths of fish, shellfish, and protists, as well as shown to reduce the viability and growth of bacteria.
[69] In addition, Fontana et al.[70] suggested that the interaction of ROS and diatom exudates (such as fatty acid hydroperoxides) are responsible for inhibiting embryonic development and causing larval abnormalities in copepods.