Dehydration is the most crucial environmental factor that limits plant growth, development, and productivity affecting agriculture throughout the world. Studies on genetic variations for dehydration tolerance in plants is crucial because divergent cultivars with contrasting traits aid the identification of key cellular components that confer better adaptability. The extracellular matrix (ECM) is a dynamic structure that serves as the repository for important signaling components and acts as a front-line defense. To better understand dehydration adaptation, a proteomic study was performed on the extracellular matrix of ICCV-2, a dehydration-susceptible genotype of chickpea. The proteome was generated with ECM-enriched fractions using two-dimensional gel electrophoresis. The LC-ESI-MS/MS analysis led to the identification of 81 dehydration-responsive proteins. The proteome was then compared with that of JG-62, a tolerant genotype. Comparative proteomics revealed genotype-specific expression of many proteins involved in a variety of cellular functions. Further, the reversible and irreversible changes in the proteomes revealed their differing ability to recover from dehydration-induced damage. We propose that cell wall restructuring and superior homeostasis, particularly the management of reactive oxygen species, may render better dehydration-adaptation. To our knowledge, this is the first report on the comprehensive comparison of dehydration-responsive organellar proteome of two genotypes with contrasting tolerance.

Glycyrrhizin, a major constituent of licorice (Glycyrrhiza glabra) root, has been reported to ameliorate insulin resistance, hyperglycemia, dyslipidemia, and obesity in rats with metabolic syndrome. Liver dysfunction is associated with this syndrome. The objective of this study is to investigate the effect of glycyrrhizin treatment on metabolic syndrome-induced liver damage. After induction of metabolic syndrome in rats by high fructose (60%) diet for 6 weeks, the rats were treated with glycyrrhizin (50 mg/kg body weight, single intra-peritoneal injection). After 2 weeks of treatment, rats were sacrificed to collect blood samples and liver tissues. Compared to normal, elevated activities of serum alanine transaminase, alkaline phosphatase and aspartate transaminase, increased levels of liver advanced glycation end products, reactive oxygen species, lipid peroxidation, protein carbonyl, protein kinase Cα, NADPH oxidase-2, and decreased glutathione cycle components established liver damage and oxidative stress in fructose-fed rats. Activation of nuclear factor κB, mitogen-activated protein kinase pathways as well as signals from mitochondria were found to be involved in liver cell apoptosis. Increased levels of cyclooxygenase-2, tumor necrosis factor, and interleukin-12 proteins suggested hepatic inflammation. Metabolic syndrome caused hepatic DNA damage and poly-ADP ribose polymerase cleavage. Fluorescence-activated cell sorting using annexin V/propidium iodide staining confirmed the apoptotic hepatic cell death. Histology of liver tissue also supported the experimental findings. Treatment with glycyrrhizin reduced oxidative stress, hepatic inflammation, and apoptotic cell death in fructose-fed rats. The results suggest that glycyrrhizin possesses therapeutic potential against hepatocellular damage in metabolic syndrome.

24‐Hydroxycholesterol (cerebrosterol, cholest‐5‐ene‐3β;, 24ξ‐diol) occurs at low levels in human (Di Frisco, De Ruggieri and Ercoli, 1953; Ercoli and De Ruggieri, 1953a, 19536; Schubert, Rose and Burger, 1961; Van Lier and Smith, 1969, 1970), equine (Ercoli, Di Frisco and De Ruggieri, 1953a; Ercoli and De Ruggieri, 1953a, 1953b; Fieser, Huang and Bhattacharyya, 1957) and bovine (Richter and Dannenberg, 1969) brain tissue. Only one of two possible C‐24 epimeric alcohols appears to occur in human brain (Van Lier and Smith, 1970) and the sterol may be regarded as a true endogenous trace‐level sterol and not as an artifact of autoxidation derived during isolation and analysis. As a phase of our continuing interests in the presence of trace‐level polar sterols in human tissues (Van Lier and Smith, 1967, 1969, 1970, 1971a; Smith and Van Lier, 1970), we sought to measure levels of 24‐hydroxycholesterol in different parts of human brain by gas chromatographic means. The present report deals with our measurements of 24‐hydroxycholesterol in human cortex, subcortical white matter, midbrain, pons, and cerebellum.