Stress induced lipid production in Chlorella vulgaris: relationship with specific intracellular reactive species levels.

Microalgae have significant potential to be an important alternative energy source, but the challenges to the commercialization of bio-oil from microalgae need to be overcome for the potential to be realized. The application of stress can be used to improve bio-oil yields from algae. Nevertheless, the understanding of stress effects is fragmented due to the lack of a suitable, direct quantitative marker for stress. The lack of understanding seems to have limited the development of stress based strategies to improve bio-oil yields, and hence the commercialization of microalgae-based bio-oil. In this study, we have proposed and used the specific intracellular reactive species levels (siROS) particularly hydroxyl and superoxide radical levels, separately, as direct, quantitative, markers for stress, irrespective of the type of stress induced. Although ROS reactions are extremely rapid, the siROS level can be assumed to be at pseudo-steady state compared to the time scales of metabolism, growth and production, and hence they can be effective stress markers at particular time points. Also, the specific intracellular (si-) hydroxyl and superoxide radical levels are easy to measure through fluorimetry. Interestingly, irrespective of the conditions employed in this study, that is, nutrient excess/limitation or different light wavelengths, the cell concentrations are correlated to the siROS levels in an inverse power law fashion. The composite plots of cell concentration (y) and siROS (x) yielded the correlations of y = k1 · x(-0.7) and y = k2 · x(-0.79) , for si-hydroxyl and si-superoxide radical levels, respectively. The specific intracellular (si-) neutral lipid levels, which determine the bio-oil productivity, are related in a direct power law fashion to the specific hydroxyl radical levels. The composite plot of si-neutral lipid levels (z) and si-hydroxyl radical level (x) yielded a correlation of z = k3 · x(0.65) . More interestingly, a nutrient shift caused a significant change in the sensitivity of neutral lipid accumulation to the si-hydroxyl radical levels.

Annonaceous acetogenins as promising DNA methylation inhibitors to prevent and treat leukemogenesis - an in silico approach.

Leukemia is a haematological malignancy affecting blood and bone marrow, ranking 10th among the other common cancers. DNA methylation is an epigenetic dysregulation that plays a critical role in leukemogenesis. DNA methyltransferases (DNMTs) such as DNMT1, DNMT3A and DNMT3B are the key enzymes catalysing DNA methylation. Inhibition of DNMT1 with secondary metabolites from medicinal plants helps reverse DNA methylation. The present study focuses on inhibiting DNMT1 protein (PDB ID: 3PTA) with annonaceous acetogenins through in-silico studies. The docking and molecular dynamic (MD) simulation study was carried out using Schrödinger Maestro and Desmond, respectively. These compounds' drug likeliness, ADMET properties and bioactivity scores were analysed. About 76 different acetogenins were chosen for this study, among which 17 showed the highest binding energy in the range of -8.312 to -10.266 kcal/mol. The compounds with the highest negative binding energy were found to be annohexocin (-10.266 kcal/mol), isoannonacinone (-10.209 kcal/mol) and annonacin (-9.839 kcal/mol). MD simulation results reveal that annonacin remains stable throughout the simulation time of 100 ns and also binds to the catalytic domain of DNMT1 protein. From the above results, it can be concluded that annonacin has the potential to inhibit the DNA methylation process and prevent leukemogenesis.Communicated by Ramaswamy H. Sarma.

Effects of microplastics, pesticides and nano-materials on fish health, oxidative stress and antioxidant defense mechanism.

Microplastics and pesticides are emerging contaminants in the marine biota, which cause many harmful effects on aquatic organisms, especially on fish. Fish is a staple and affordable food source, rich in animal protein, along with various vitamins, essential amino acids, and minerals. Exposure of fish to microplastics, pesticides, and various nanoparticles generates ROS and induces oxidative stress, inflammation, immunotoxicity, genotoxicity, and DNA damage and alters gut microbiota, thus reducing the growth and quality of fish. Changes in fish behavioral patterns, swimming, and feeding habits were also observed under exposures to the above contaminants. These contaminants also affect the Nrf-2, JNK, ERK, NF-κB, and MAPK signaling pathways. And Nrf2-KEAP1 signalling modulates redox status marinating enzymes in fish. Effects of pesticides, microplastics, and nanoparticles found to modulate many antioxidant enzymes, including superoxide dismutase, catalase, and glutathione system. So, to protect fish health from stress, the contribution of nano-technology or nano-formulations was researched. A decrease in fish nutritional quality and population significantly impacts on the human diet, influencing traditions and economics worldwide. On the other hand, traces of microplastics and pesticides in the habitat water can enter humans by consuming contaminated fish which may result in serious health hazards. This review summarizes the oxidative stress caused due to microplastics, pesticides and nano-particle contamination or exposure in fish habitat water and their impact on human health. As a rescue mechanism, the use of nano-technology in the management of fish health and disease was discussed.

Simultaneous increases in specific growth rate and specific lipid content of Chlorella vulgaris through UV-induced reactive species.

A challenge in algae-based bio-oil production is to simultaneously enhance specific growth rates and specific lipid content. We have demonstrated simultaneous increases in both the above in Chlorella vulgaris through reactive species (RS) induced under ultraviolet (UV) A and UVB light treatments. We postulated that the changes in photosystem (PS) stoichiometry and antenna size were responsible for the increases in specific growth rate. UVB treatment excited PSII, which resulted in a twofold to sevenfold increase in PSII/PSI ratio compared to control. An excited PSII caused a 2.7-fold increase in the specific levels of superoxide and a twofold increase in the specific levels of hydroxyl radicals. We have established that the increased specific intracellular RS (si-RS) levels increased the PSII antenna size by a significant 10-fold as compared to control. In addition, the 8.2-fold increase in specific lipid content was directly related to the si-RS levels. We have also demonstrated that the RS induced under UVA treatment led to a 3.2-fold increase in the saturated to unsaturated fatty acid ratio. Based on the findings, we have proposed and demonstrated a UV-based strategy, which achieved an 8.8-fold increase in volumetric lipid productivity.

UVA-induced reset of hydroxyl radical ultradian rhythm improves temporal lipid production in Chlorella vulgaris.

We report for the first time that the endogenous, pseudo-steady-state, specific intracellular levels of the hydroxyl radical (si-OH) oscillate in an ultradian fashion (model system: the microalga, Chlorella vulgaris), and also characterize the various rhythm parameters. The ultradian rhythm in the endogenous levels of the si-OH occurred with an approximately 6 h period in the daily cycle of light and darkness. Further, we expected that the rhythm reset to a shorter period could rapidly switch the cellular redox states that could favor lipid accumulation. We reset the endogenous rhythm through entrainment with UVA radiation, and generated two new ultradian rhythms with periods of approximately 2.97 h and 3.8 h in the light phase and dark phase, respectively. The reset increased the window of maximum lipid accumulation from 6 h to 12 h concomitant with the onset of the ultradian rhythms. Further, the saturated fatty acid content increased approximately to 80% of total lipid content, corresponding to the peak maxima of the hydroxyl radical levels in the reset rhythm.