scholarly journals Metabolic transformation of selenium (IV) by bacteria of the genus Azospirillum

Author(s):  
A. V. Tugarova ◽  
P. V. Mamchenkova ◽  
A. A. Kamnev

Possible mechanisms of selenite reduction by bacteria of the genus Azospirillum are studied. A method is proposed for producing extracellular Se nanoparticles homogeneous by size which have been characterised by various methods.

1988 ◽  
Vol 15 (3) ◽  
pp. 219-223
Author(s):  
Jørgen Clausen ◽  
Søren Achim Nielsen

The mixed-function oxygenase system involved in the metabolism of drugs and xenobiotics has been extensively studied in various animal species and in various organs (1). It is now apparent that in humans the p-450 complex is one representative of a related family, expressed by 13 c-DNA genes showing approximately 36% similarity between the different subfamilies (2). In order to compare the in vivo and in vitro metabolic effects of drugs and xenobiotics, the induction capabilities of the mixed-function oxygenase must be known. The most sensitive non-isotopic assay system for determination of mixed-function oxygenase activity is the method of Nebert & Gelboin (3,4), which is based on the metabolic transformation of benzo-(a)-pyrene to its fluorescent hydroxyl derivatives (5). However, the levels of the mixed-function oxygenase enzymes in different cellular systems show great variations, with the highest activities in liver cells. Therefore, in order to use human lymphocytes and other cellular systems with low mixed-function oxygenase activities, the assay method for determining oxygenase activity must have the highest possible sensitivity. The present communication is devoted to a study aimed at increasing the sensitivity of Nebert & Gelboin's methods for assay of mixed-function oxygenase subfamilies using benzo-(a)-pyrene as a substrate.


2011 ◽  
Vol 9 (4) ◽  
pp. 313-334 ◽  
Author(s):  
Stacey N. Barnaby ◽  
Stephen H. Frayne ◽  
Karl R. Fath ◽  
Ipsita A. Banerjee
Keyword(s):  

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5931 ◽  
Author(s):  
Jingming Zhao ◽  
Wencheng Yu

BackgroundCystic fibrosis (CF) is a disease characterized by chronic airway infection with a high incidence and poor prognosis.Pseudomonas aeruginosaandAspergillus fumigatusare pathogens commonly found in CF patients. Clinically, these two microorganisms often coexist in the airway of CF patients. Combined infection withP. aeruginosaandA. fumigatusresults in worsening lung function and clinical condition.MethodsIn this review, we focus on the mutual inhibition and promotion mechanisms ofP. aeruginosaandA. fumigatusin CF patients. We also summarized the mechanisms of the interaction between these pathogenic microorganisms.ResultsP. aeruginosainhibitsA. fumigatusgrowth through the effects of phenazines, the quorum sensing system, iron competition, bacteriophages, and small colony variants.P. aeruginosainducesA. fumigatusgrowth through volatile organic compounds and subbacteriostatic concentrations of phenazines.A. fumigatusinterferes withP. aeruginosa, affecting its metabolic growth via phenazine metabolic transformation, gliotoxin production, and reduced antibiotic sensitivity.DiscussionCoexistence ofP. aeruginosaandA. fumigatuscan lead to both mutual inhibition and promotion. In different stages of CF disease, the interaction between these two pathogenic microorganisms may shift between promotion and inhibition. A discussion of the mechanisms ofP. aeruginosaandA. fumigatusinteraction can be beneficial for further treatment of CF patients and for improving the prognosis of the disease.


2016 ◽  
Vol 7 (12) ◽  
pp. 4976-4983 ◽  
Author(s):  
Ou Lv ◽  
Lifang Wang ◽  
Jianke Li ◽  
Qianqian Ma ◽  
Wei Zhao

PPPs, PC and PEA in different concentrations were found to decrease the total cholesterol (TC) content and increase the total bile acid (TBA) content of a human hepatic cell model, and so possess a lipid-lowering effect.


1992 ◽  
Vol 262 (1) ◽  
pp. G1-G13 ◽  
Author(s):  
P. K. Rangachari

This review considers the possibility that histamine functions as a cellular messenger in the gastrointestinal tract. Any biological messenger must be produced, received, and responded to, and must have its actions quickly terminated. Histamine is no exception. Histamine synthesis from L-histidine occurs in enterochromaffin-like cells, mucosal mast cells, and nerves. Histamine release occurs through both antibody-dependent and antibody-independent mechanisms. Released histamine interacts with a variety of cellular targets (epithelial cells, smooth muscle cells, endothelial cells, neurons, and a variety of immunocompetent cells). Occupation of H1, H2, and H3 receptors, defined by pharmacological agents, is transduced by different intracellular messengers (Ca2+, cyclic nucleotides) into diverse effects such as secretion, contraction, or modulation of other secretagogues. The responses to histamine are terminated by at least three different mechanisms: metabolic transformation by the actions of methyltransferase and diamine oxidase, desensitization at the receptor level, and cellular uptake. In addition to its well-documented effects as a mediator of inflammatory processes, histamine may also function as a neuro- and immunoregulator. While a significant pathophysiological role for histamine has been realized since the earliest description of its effects, the availability of newer pharmacological agents has permitted a finer dissection of its "physiological" effects and raised the possibility of multiple roles for histamine.


1988 ◽  
Vol 255 (5) ◽  
pp. F984-F994 ◽  
Author(s):  
M. VanScoy ◽  
M. Loghman-Adham ◽  
M. Onsgard ◽  
M. Szczepanska-Konkel ◽  
S. Homma ◽  
...  

We examined whether phosphonoformate (PFA) can cause phosphaturia through its direct action on brush-border membrane (BBM) in vivo. Infusion of PFA or of parathyroid hormone (PTH) to thyroparathyroidectomized rats caused a marked increase in fractional excretion of phosphate without changes in excretion of Na+ or of GFR. The PFA-induced phosphaturia was not accompanied by an increase in urinary adenosine-3',5'-cyclic monophosphate (cAMP); moreover, PFA added in vitro did not influence the PTH-sensitive adenylate cyclase and cAMP-phosphodiesterase in proximal convoluted tubules. In BBM vesicles (BBMV) from rats with PFA-elicited phosphaturia, neither the rate of Na+-Pi symport nor Na+-dependent binding of [14C]PFA on BBMV was changed, whereas in BBMV from PTH-infused rats the Vmax of Na+-Pi symport decreased. PFA is almost completely ultrafiltrable; no metabolic transformation of PFA was detected after [14C]PFA exposure to rat renal cortical slices, homogenate, or to blood. We conclude that PFA causes phosphaturia by direct inhibition of Na+-Pi symport across BBM in proximal tubules, acting from the luminal side. Thus PFA (foscarnet) has a unique direct mechanism of phosphaturic effect, via its action on Pi reabsorption in proximal tubules in vivo.


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