TY - JOUR
T1 - Selenium
T2 - a potent regulator of ferroptosis and biomass production
AU - Ramakrishnan, Muthusamy
AU - Arivalagan, Jaison
AU - Satish, Lakkakula
AU - Mohan, Manikandan
AU - Samuel Selvan Christyraj, Johnson Retnaraj
AU - Chandran, Sam Aldrin
AU - Ju, Ho Jong
AU - John L, Anoopa
AU - Ramesh, Thiyagarajan
AU - Ignacimuthu, Savarimuthu
AU - Kalishwaralal, Kalimuthu
N1 - Funding Information:
This work was funded by Metasequoia Faculty Research Start-up Funding (grant number 163100028) at the Bamboo Research Institute , Nanjing Forestry University, Nanjing 210037, Jiangsu, China for first author Dr. Muthusamy Ramakrishnan. Dr. Kalimuthu Kalishwaralal was awarded by the “MK Bhan Young Researcher Fellowship program (YRFP) for 2020–2021” (Ref: No, HRD-12/4/2020-AFS-DBT ). We would like to extend our sincere gratitude and appreciation to all the reviewers for their valuable comments. The authors apologize to those whose original work(s) could not be included in this review due to space limitations. The images were created using icons from the BioRender library Biorender.com.
Publisher Copyright:
© 2022 Elsevier Ltd
PY - 2022/11/1
Y1 - 2022/11/1
N2 - Emerging evidence supports the notion that selenium (Se) plays a beneficial role in plant development for modern crop production and is considered an essential micronutrient and the predominant source of plants. However, the essential role of selenium in plant metabolism remains unclear. When used in moderate concentrations, selenium promotes plant physiological processes such as enhancing plant growth, increasing antioxidant capacity, reducing reactive oxygen species and lipid peroxidation and offering stress resistance by preventing ferroptosis cell death. Ferroptosis, a recently discovered mechanism of regulated cell death (RCD) with unique features such as iron-dependant accumulation of lipid peroxides, is distinctly different from other known forms of cell death. Glutathione peroxidase (GPX) activity plays a significant role in scavenging the toxic by-products of lipid peroxidation in plants. A low level of GPX activity in plants causes high oxidative stress, which leads to ferroptosis. An integrated view of ferroptosis and selenium in plants and the selenium-mediated nanofertilizers (SeNPs) have been discussed in more recent studies. For instance, selenium supplementation enhanced GPX4 expression and increased TFH cell (Follicular helper T) numbers and the gene transcriptional program, which prevent lipid peroxidase and protect cells from ferroptosis. However, though ferroptosis in plants is similar to that in animals, only few studies have focused on plant-specific ferroptosis; the research on ferroptosis in plants is still in its infancy. Understanding the implication of selenium with relevance to ferroptosis is indispensable for plant bioresource technology. In this review, we hypothesize that blocking ferroptosis cell death improves plant immunity and protects plants from abiotic and biotic stresses. We also examine how SeNPs can be the basis for emerging unconventional and advanced technologies for algae/bamboo biomass production. For instance, algae treated with SeNPs accumulate high lipid profile in algal cells that could thence be used for biodiesel production. We also suggest that further studies in the field of SeNPs are essential for the successful application of this technology for the large-scale production of plant biomass.
AB - Emerging evidence supports the notion that selenium (Se) plays a beneficial role in plant development for modern crop production and is considered an essential micronutrient and the predominant source of plants. However, the essential role of selenium in plant metabolism remains unclear. When used in moderate concentrations, selenium promotes plant physiological processes such as enhancing plant growth, increasing antioxidant capacity, reducing reactive oxygen species and lipid peroxidation and offering stress resistance by preventing ferroptosis cell death. Ferroptosis, a recently discovered mechanism of regulated cell death (RCD) with unique features such as iron-dependant accumulation of lipid peroxides, is distinctly different from other known forms of cell death. Glutathione peroxidase (GPX) activity plays a significant role in scavenging the toxic by-products of lipid peroxidation in plants. A low level of GPX activity in plants causes high oxidative stress, which leads to ferroptosis. An integrated view of ferroptosis and selenium in plants and the selenium-mediated nanofertilizers (SeNPs) have been discussed in more recent studies. For instance, selenium supplementation enhanced GPX4 expression and increased TFH cell (Follicular helper T) numbers and the gene transcriptional program, which prevent lipid peroxidase and protect cells from ferroptosis. However, though ferroptosis in plants is similar to that in animals, only few studies have focused on plant-specific ferroptosis; the research on ferroptosis in plants is still in its infancy. Understanding the implication of selenium with relevance to ferroptosis is indispensable for plant bioresource technology. In this review, we hypothesize that blocking ferroptosis cell death improves plant immunity and protects plants from abiotic and biotic stresses. We also examine how SeNPs can be the basis for emerging unconventional and advanced technologies for algae/bamboo biomass production. For instance, algae treated with SeNPs accumulate high lipid profile in algal cells that could thence be used for biodiesel production. We also suggest that further studies in the field of SeNPs are essential for the successful application of this technology for the large-scale production of plant biomass.
KW - Algae
KW - Ferroptosis
KW - Lipid peroxidase
KW - Nanoparticles
KW - Selenium accumulation
KW - Selenium fertilization
KW - Selenium-induced
UR - http://www.scopus.com/inward/record.url?scp=85133764854&partnerID=8YFLogxK
U2 - 10.1016/j.chemosphere.2022.135531
DO - 10.1016/j.chemosphere.2022.135531
M3 - Article
C2 - 35780987
AN - SCOPUS:85133764854
VL - 306
JO - Chemosphere
JF - Chemosphere
SN - 0045-6535
M1 - 135531
ER -