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Snake venom contains a diverse array of proteins and polypeptides. Cytotoxins and short neurotoxins are non-enzymatic
polypeptide components of snake venom. The three-dimensional structure of cytotoxin and short neurotoxin resembles a three
finger appearance of three-finger protein super family. Different family members of three-finger protein super family are employed
in diverse biological functions. In this work we analyzed the cytotoxin, short neurotoxin and related non-toxin proteins of other
chordates in terms of functional analysis, amino acid compositional (%) profile, number of amino acids, molecular weight,
theoretical isoelectric point (pI), number of positively charged and negatively charged amino acid residues, instability index and
grand average of hydropathy with the help of different bioinformatical tools. Among all interesting results, profile of amino acid
composition (%) depicts that all sequences contain a conserved cysteine amount but differential amount of different amino acid
residues which have a family specific pattern. Involvement in different biological functions is one of the driving forces which
contribute the vivid amino acid composition profile of these proteins. Different biological system dependent adaptation gives the
birth of enriched bio-molecules. Understanding of physicochemical properties of these proteins will help to generate medicinally
important therapeutic molecules for betterment of human lives. 相似文献
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Sao Dilip Das Sandip Pramanik Subhamay Kuiri Probodh K. Nath Rajib 《Plasmonics (Norwell, Mass.)》2021,16(4):1319-1326
Plasmonics - The interplaying role of particle size and polymer layer thickness on the tunable optical response of polymer-coated Ag nanoparticles (NPs) has been studied experimentally and... 相似文献
3.
Snakes are equipped with their venomic armory to tackle different prey and predators in adverse natural world. The venomic
composition of snakes is a mix of biologically active proteins and polypeptides. Among different components snake venom
cytotoxins and short neurotoxin are non-enzymatic polypeptide candidates with in the venom. These two components structurally
resembled to three-finger protein superfamily specific scaffold. Different non-toxin family members of three-finger protein
superfamily are involved in different biological roles. In the present study we analyzed the snake venom cytotoxins, short
neurotoxins and related non-toxin proteins of different chordates in terms of amino acid sequence level diversification profile,
polarity profile of amino acid sequences, conserved pattern of amino acids and phylogenetic relationship of these toxin and nontoxin
protein sequences. Sequence alignment analysis demonstrates the polarity specific molecular enrichment strategy for better
system adaptivity. Occurrence of amino acid substitution is high in number in toxin sequences. In non-toxin body proteins there
are less amino acid substitutions. With the help of conserved residues these proteins maintain the three-finger protein scaffold. Due
to system specific adaptation toxin and non-toxin proteins exhibit a varied type of amino acid residue distribution in sequence
stretch. Understanding of Natural invention scheme (recruitment of venom proteins from normal body proteins) may help us to
develop futuristic engineered bio-molecules with remedial properties. 相似文献
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Aparajita Ghosh Ardhendu K. Mandal Sibani Sarkar Subhamay Panda Nirmalendu Das 《Life sciences》2009,84(3-4):75-80
AimsThis study was performed to evaluate the therapeutic efficacy of nanocapsulated flavonoidal quercetin (QC) in combating arsenic-induced reactive oxygen species (ROS)-mediated oxidative damage in hepatocytes and brain cells in a rat model.Main methodsHepatic and neuronal cell damage in rats was made by a single injection (sc) of sodium arsenite (NaAsO2, 13 mg/kg b. wt. in 0.5 ml of physiological saline). A single dose of 500 µl of quercetin suspension (QC) (QC 8.98 µmol/kg) or 500 µl of nanocapsulated QC (NPQC) (QC 8.98 µmol/kg) was given orally to rats at 90 min prior to the arsenite injection.Key findingsInorganic arsenic depositions (182 ± 15.6 and 110 ± 12.8 ng/g protein) were found in hepatic and neuronal mitochondrial membranes. Antioxidant levels in hepatic and neuronal cells were reduced significantly by arsenic. NPQC prevented the arsenite-induced reduction in antioxidant levels in the liver and brain. Arsenic induced a substantial decrease in liver and brain cell membrane microviscosities, and NPQC treatment resulted in a unique protection against the loss. A significant correlation between mitochondrial arsenic and its conjugated diene level was observed both in liver and brain cells for all experimental rats.SignificanceArsenic-specific antidotes are used against arsenic-induced toxicity. However, the target site is poorly recognized and therefore achieving an active concentration of drug molecules can be a challenge. Thus, our objective was to formulate NPQC and to investigate its therapeutic potential in an oral route against arsenite-induced hepatic and neuronal cell damage in a rat model. 相似文献
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Ghosh S Wilson MR Choudhury S Yamamoto H Goddard ME Falusi B Marczin N Takata M 《American journal of physiology. Lung cellular and molecular physiology》2005,288(6):L1003-L1009
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are major causes of morbidity and mortality in the intensive care unit, but despite continuing research few effective therapies have been identified. In recent years, inhaled carbon monoxide (CO) has been reported to have cytoprotective effects in several animal models of tissue injury. We therefore evaluated the effects of inhaled CO in three different in vivo mouse models of ALI. Anesthetized C57BL/6 mice were ventilated with oxygen in the presence or absence of CO (500 parts per million) for 1 h before lung injury was induced by lipopolysaccharide (LPS) or oleic acid (OA) administration. Ventilation was then continued with the same gases for a further 2-3 h, with hemodynamic and respiratory parameters monitored throughout. Intratracheal LPS administration induced lung injury with alveolar inflammation (increased lavage fluid neutrophils, total protein, and cytokines). In contrast, intravenous LPS induced a predominantly vascular lung injury, with increased plasma TNF and increased neutrophil activation (surface Mac-1 upregulation and L-selectin shedding) and sequestration within the pulmonary vasculature. Intravenous OA produced deteriorations in lung function, reflected by changes in respiratory mechanics and blood gases and lavage fluid neutrophil accumulation. However, addition of CO to the inspired gas did not produce significant changes in the measured physiological or immunological parameters in the mouse models used in this study. Thus the results do not support the hypothesis that use of inhaled CO is beneficial in the treatment of ALI and ARDS. 相似文献
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