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Guar korma and churi protein isolates were assessed for their physicochemical, nutritional, functional, structural, and digestibility properties for their application in the food industry. The water extracted protein isolate of guar korma showed a protein content of 89.7 % and a yield of 48.7 %. Water extracted protein isolate of guar korma showed an excellent protein efficiency ratio, essential amino acid/total amino acids (34.35 %), amino acid score, and protein digestibility corrected amino acid score values, suggesting the existence of high-quality proteins. Water extracted protein isolate of guar korma contains all the essential amino acids except Methionine and Cysteine, according to World Health Organization recommendations for children and adults. The protein profiling of water extracted protein isolate of guar korma was analyzed using 12 % sodium dodecyl sulfate polyacrylamide gel electrophoresis and indicated the presence of eight major protein bands in the range of 17–100 kDa. In vitro digestibility of water extracted protein isolate of guar korma showed the complete digestion of the abundant protein bands within 15 min. Further, the foaming capacity, water/oil holding capacity, and emulsifying stability of water extracted protein isolate of guar korma were comparable with soy protein isolate. Fourier Transform Infrared and Circular Dichroism spectral analysis revealed the presence of several aromatic groups and β-sheets, random coils respectively in water extracted protein isolate of guar korma. The morphological nature of the guar protein isolate was characterized by Scanning Electron Microscopy. Overall, these findings support that water extracted protein isolate of guar korma has excellent functional and nutritional properties and could be a potential alternative plant protein in food industries.

Diacylglycerol (DAG) oil is suggested to have anti-obesity effect in view of its distinct metabolic fate and fat oxidation. In the present investigation, dietary feeding of DAG rich sunflower and rice bran oils for 12 weeks in Wistar rats significantly decreased triacylglycerol (TAG), total cholesterol and LDL-cholesterol in serum, liver and adipose. Fat accumulation was decreased in DAG fed groups. Fecal cholesterol levels increased in DAG fed rats. DAG rich oil decreased selected cardiovascular disease (CVD) risk factors such as serum C-reactive protein (C-RP), tumor necrosis factor-alpha (TNF-α), platelet aggregation and expression of thoracic aortic proteins such as inducible nitric oxide synthase (i-NOS), cyclooxygenase-2 (COX-2), and vascular cell adhesion molecule-1 (VCAM-1) compared to TAG oil fed group. Serum clinical enzyme activity and histopathological observations of liver conforms safety of DAG oil. Thus, DAG rich oil has beneficial metabolic effects by decreasing fat accumulation, lipid profile and CVD risk factors.

Tobacco products and cigarette smoke cause many respiratory diseases including cancer. 4-(Methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent carcinogen in cigarette smoke, but its effect on lipid metabolism remains enigmatic. Hence, Saccharomyces cerevisiae was exposed to different concentrations of NNK (0-400 µmol L-1) to elucidate its role in lipid metabolism. Exposure to NNK substantially decreases (about 60%) of the phospholipid content with a concomitant increase in lysophospholipids. Significant reduction was observed in the phosphatidylcholine followed by phosphatidylethanolamine with NNK-treated cells. On the contrary, cells accumulated significant amount of neutral lipids and free fatty acids. Exposure of yeast cells (wild-type cells and three plbΔ mutant strains) to NNK greatly enhances the hydrolysis of phospholipid in the presence of calcium. We are the first to report that exposure to NNK enhances phospholipase B (PLB), particularly plb1p activity. Furthermore, NNK also promotes the alteration of phospholipid fatty acid (FA) content. These results suggest that NNK aids in the degradation of phospholipids by enhanced PLB activity and is accompanied with FA alteration. Understanding the altered phospholipid metabolism in the presence of NNK remains a worthy pursuit. [ABSTRACT FROM AUTHOR]

Lipopolysaccharide (LPS) is an endotoxin, a potent stimulator of immune response and induction of LPS leads to acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). ARDS is a life-threatening disease worldwide with a high mortality rate. The immunological effect of LPS with spleen and thymus is well documented; however the impact on membrane phospholipid during endotoxemia has not yet been studied. Hence we aimed to investigate the influence of LPS on spleen and thymus phospholipid and fatty acid composition by [(32) P]orthophosphate labeling in rats. The in vitro labeling was carried out with phosphate-free medium (saline). Time course, LPS concentration-dependent, pre- and post-labeling with LPS and fatty acid analysis of phospholipid were performed. Labeling studies showed that 50 µg LPS specifically altered the major phospholipids, phosphatidylcholine and phosphatidylglycerol in spleen and phosphatidylcholine in thymus. Fatty acid analysis showed a marked alteration of unsaturated fatty acids/saturated fatty acids in spleen and thymus leading to immune impairment via the fatty acid remodeling pathway. Our present in vitro lipid metabolic labeling study could open up new vistas for exploring LPS-induced immune impairment in spleen and thymus, as well as the underlying mechanism., (Copyright © 2011 John Wiley & Sons, Ltd.)

Acute lung injury (ALI) or its severe form, acute respiratory distress syndrome (ARDS) is an important cause of mortality in the human population. Despite significant advances made, the mortality associated with ALI remains unchanged. The objective of the present study was to evaluate the role of oxidative stress, alveolar antioxidant status and multiple organ injury in ARDS induced by lipopolysaccharide (LPS) in rats. Rats were divided into 4 groups, group I control rats were given saline intraperitoneally, whereas groups II, III and IV (LPS-treated) rats received an intraperitoneal injection of LPS (10 mg/kg body weight) and sacrificed after various time intervals. In LPS-treated rats, we observed increased levels of oxidative products, decreased levels of antioxidants in lung tissues and increased levels of serum marker enzymes, suggesting multiple organ injury. Bronchoalveolar lavage fluid (BALF) neutrophil content and protein concentration in LPS-treated rats were significantly elevated in a time-dependent manner. Histological studies revealed neutrophil influx and diffused alveolar damage in LPS-administered rats. These results clearly suggested that increased oxidant levels led to oxidative stress, antioxidant deficiency attenuating lung inflammation and tissue damage. LPS administration resulted in multiple organ failure, leading to increased mortality.