Nanoceria

High temperature represents one of the most serious abiotic stress factors limiting plant photosynthesis, biomass production and crop productivity. Photosynthetic apparatus is an important heat sensor in plants, sensing a wide range of air temperatures, from moderate to extreme. In this chapter we offer current knowledge on both photochemical and metabolic changes occurring within the photosynthetic apparatus in conditions of heat stress associated with signaling and stress response. The heat stress directly affects the heat sensitive sites, mainly Oxygen Evolving Complex of Photosystem II and Rubisco activase. It leads to subsequent indirect effects, such as changes of the redox status of individual components on thylakoid membrane in chloroplast and increase in production of Reactive Oxygen Species (ROS). Hence, the redox signaling plays the crucial role in enhancement of alternative electron pathways such as cyclic electron flow as well as triggering the signal transduction pathways resulting to heat stress response. The redox signaling in chloroplast is closely associated with ROS signaling, which interferes with regulation also out of chloroplast. The stress response involves mainly production of specific proteins (mostly heat shock proteins or antioxidants) or protective compounds (osmoprotectants) leading to increase of thermostability of sensitive sites or protection against ROS. Different signal molecules contribute in photosynthesis-related heat-stress signaling pathways, such as reactive oxygen species with hydrogen peroxide, nitric oxide, calcium, abscisic acid, etc. The specific roles of cytokinins and isoprene in heat stress response are also reviewed.

Ceria nanoparticles (nano-CeO2), due to their widespread applications, have attracted a lot of concern about their toxic effects on both human health and the environment. The present work aimed to evaluate the in vivo effects of nano- CeO2 (8.5 nm) on Caenorhabditis elegans (C. elegans) at environmental relevant concentrations (molar concentrations ranging from 1 nM to 100 nM). The results indicate that nano- CeO2 could induce ROS accumulation and oxidative damage in C. elegans, and finally lead to a decreased lifespan. The most surprising thing is that the mean lifespan of nematodes was significantly decreased by 12% even at the exposure level of 1 nM (p < 0.01). In vitro tests suggest that the ability of nano- CeO2 to catalyze ROS generation was involved in the mechanism for its toxicity to C. elegans. To our best knowledge, this is the first case in which nanoparticles exhibit adverse effects on organisms at such low concentrations (1nM-100 nM). So, our findings indicate the importance of nanotoxicological investigations at environmentally relevant concentrations and will attract more attentions on the risks of NPs exposure.

Objective: Cyclophosphamide (CP), as an anticancer agent has side effects, especially hepatotoxicity. Cerium oxide nanopar-ticles [nanoceria (NC)], which act as antioxidants, have a protective effect against oxidative stress-induced toxicity. This study evaluated the preventive effect of NC in hepatotoxicity induced by CP. Materials and Methods: Thirty-two mice were randomly distributed into four groups: control (received only normal saline), NC (received NC 100 μg/kg for 3 days, intraperitoneally), CP (received CP 200 mg/kg single dose on the third day of the study, intraperitoneally), and NC+CP (NC 100 μg/kg and CP 200 mg/kg). Two days after the final treatment, oxidative stress marker (MDA and GSH) and alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phos-phatase (ALP) levels were measured, and histopathological and immunohistochemical examinations were performed for determining the effects of NC on hepatotoxicity. Results: CP-induced hepatotoxicity was evident by the significant elevation of liver enzyme levels and alteration in oxidative stress marker levels. Additionally, histopathological changes and apoptosis were markedly increased. NC decreased MDA level, increased GSH level and decreased liver enzyme levels in CP-treated mice. In addition, NC pretreatment could be alleviated by the immunoreactivity of caspase-3 in CP-treated mice compared with the CP group. Conclusion: NC showed a potent antioxidant effect in hepatotoxicity induced by CP. The study suggested that NC through its antioxidant and anti-apoptotic properties has a protective effect against hepatotoxicity induced by CP.