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Reaction Centers as Nanoscale Photovoltaic Devices
Published in Swee Ching Tan, Photosynthetic Protein-Based Photovoltaics, 2018
The aim of this chapter has been to provide a basic introduction to the three types of photochemical RC that have been utilized for bio-photovoltaics. Between them they cover a major part of the useable solar spectrum and span the range of reduction potential that living systems occupy. These natural materials have many attractive attributes but also present challenges for use in a device setting. As an example, photosystems that operate at extremes of redox potential are prone to photooxidative damage; as they are integral membrane proteins, they also can exhibit limited stability following isolation from the host organism. This is a particular issue for PSII, which generates extremes of oxidizing potential to convert water to oxygen and which is continually repaired by replacement of the D1 protein. It is noticeable that the bulk of studies into RC photovoltaics have concerned PSI or purple bacterial photoproteins, and the limited photostability of PSII in vitro has been a factor in this. Although stability is an issue at present, the field of RC photovoltaics is still in its infancy and is developing rapidly, and it will be fascinating to see where the exploitation of natural photosynthetic materials in biohybrid devices leads.
Algal photobiohydrogen production
Published in Ozcan Konur, Bioenergy and Biofuels, 2017
Archana Tiwari, Thomas Kiran, Anjana Pandey
The starvation of sulfur enhances hydrogen production as reported in Gloeocapsa alpicola and Synechocystis PCC 6803 (Antal and Lindbad, 2005). It is possible to inhibit the oxygenic photosynthesis and enhance hydrogen production by incubating in nutrients that lack sulfur. Sulfur is a very important component in the Photosystem II (PSII) repair cycle, and without sulfur the protein biosynthesis is greatly impaired and production of either cysteine or methionine becomes impossible. This results in a lack of the D1 protein (32-kDa reaction center protein), which is essential for Photosystem II and needs to be constantly replaced. For these reasons, during sulfur deprivation photosynthesis and respiration decrease, even in the presence of light. Because photosynthesis declines much quicker than respiration, an equilibrium point is reached after a while (usually after 22 h) and after that the amount of oxygen that is used in respiration is greater than the oxygen released by photosynthesis and the cell become anaerobic and at this point hydrogen production occurs in higher amounts, reaching peak production.
Introduction
Published in Donat-P. Häder, Kunshan Gao, Aquatic Ecosystems in a Changing Climate, 2018
Many exposed organisms have developed strategies to mitigate UV-induced damage by self-shading in crusts or by vertical migration out of the danger zone (Häder et al. 2015, Häder and Horneck 2018). In addition, both prokaryotic and eukaryotic primary producers have developed UV-absorbing substances, such as scytonemin (found only in cyanobacteria) or mycosporine-like amino acids (MAAs, in prokaryotic and eukaryotic phytoplankton and in many macroalgae) which are deposited outside the cell or in outer layers so that damaging radiation is attenuated before it can reach the nucleus and produce damage (Rastogi et al. 2014, Richa et al. 2016, Pandey et al. 2017). In contrast, many consumers do not possess the Shikimate pathway to produce MAAs but can ingest the substances with their diet and utilize them for the same purpose (Ekvall et al. 2015). Extracellularly and intracellularly produced ROS is quenched by enzymatic or non-enzymatic mechanisms to mitigate solar UV- B damage (Häder et al. 2015, Li et al. 2017). A final method to reduce UV damage is the use of efficient repair mechanisms (Sinha and Häder 2002, Chang et al. 2017). UV-B is known to induce cyclobutane pyrimidine dimers (CPD) which are repaired by photolyases (MacFadyen et al. 2004, Häder and Sinha 2005). However, these repair mechanisms are not foolproof so that mutations and genetic aberrations occur resulting in increased mortality (Lesser and Barry 2003, Häder et al. 2007). The damage of the vital D1 protein in photosystem II, essential for the photosynthetic electron transport, is repaired by a fast and efficient resynthesis—replacing the damaged protein with a new copy (Wong et al. 2015, Wu et al. 2015).
Non-stomatal limitation of photosynthesis by soil salinity
Published in Critical Reviews in Environmental Science and Technology, 2021
Ting Pan, Minmin Liu, Vladimir D. Kreslavski, Sergey K. Zharmukhamedov, Chenrong Nie, Min Yu, Vladimir V. Kuznetsov, Suleyman I. Allakhverdiev, Sergey Shabala
In higher plants the susceptibility of PSII to high light stress (photoinhibition) is associated with the degradation of the D1 protein (Aro, Virgin, & Andersson, 1993). PSII D1 protein is the most important in process of the repair of photodamaged of PSII. Speaking in detail, specific light-induced proteases are required for removing damaged D1 protein which is replaced with a new copy produced by de novo synthesis (Yamamoto, 2016) in a process termed reversible photoibhibition. However, at very high irradiance the D1 aggregation is occurred and D1 replacement is limited due to interaction of D1 with proteases is difficult, and PSII inhibition is getting irreversible. It should be also noted that both the reversible and irreversible photoinhibition are dependent on the membrane fluidity of the thylakoids. At the molecular level, salt stress affects the repair via inhibiting the expression of the psbA genes for preD1, at both transcriptional and the translational levels (Allakhverdiev et al., 2002, Figure 1). Salt stress also inhibited degradation of D1 protein in the photodamaged PSII. Similar results were also reported for higher plants (reviewed in Murata et al., 2012; Jajoo, 2014).
Toxicological sensitivity of Pennisetum americanum (L.) K. Schum to atrazine exposure
Published in International Journal of Phytoremediation, 2018
Zhao Jiang, Guangxia Su, Jinmei Li, Bingbing Ma, Yukun Chen, Dexin Shan, Ying Zhang
However, atrazine has been reported to exhibit biotoxicity toward many non-target organisms, even at ppb (parts per billion, μg/L or μg/kg) concentrations (Hayes et al. 2010; Sanderson et al. 2000, 2001). Therefore, atrazine threshold value in ground and drinking water of Europe and North America must not exceed 0.1 μg/L (Vonberg et al. 2014). In addition, phytotoxicity studies have shown that atrazine can inhibit the elongation and biomass of sensitive plants after being absorbed by the roots (Su and Zhu, 2007; Tang et al. 1997). This toxicity was due in part to damage to photosystem II (PSII) of sensitive plants; atrazine could inhibit photosynthesis by displacing the secondary quinone acceptor of the electron transport chain from its binding site (Gao et al. 2011). As a result, the D1 protein, which forms a heterodimer with the D2 protein in the reaction center of PSII, was degraded rapidly and chlorophyll synthesis was affected accordingly (Sen et al. 2014, Zhang et al. 2014). Therefore, atrazine has been selected as a model toxicant in phytotoxicity studies. In addition, atrazine can cause oxidative stress to cell membranes, resulting in cell damage or death (Akbulut and Yigit, 2010; Liu et al. 2013). Additionally, as it has a long residual period and high mobility, atrazine can be detected in soil, surface water, and groundwater years after its initial application (Stipičević et al. 2015). Therefore, the increasing residual amount of atrazine in both soil and water poses a significant threat to environment safety.