Cellular Defense Enzyme Profile for Non-cytotoxic and Phenol Enriched Extracts of Heliotropium europaeum, Carlina oligocephala and Echinops ritro

2018 ◽  
Vol 14 (2) ◽  
pp. 224-238
Author(s):  
Belgin S. Isgor ◽  
Yasemin G. Isgor ◽  
Fatmagul Geven
Keyword(s):  
Enzyme Profile ◽  
Cellular Defense ◽  
Defense Enzyme ◽  
Heliotropium Europaeum

Effect of Cereal Cyst Nematode Infection on Defense Enzyme Activity of Wheat Root

2012 ◽  
Vol 18 (3) ◽  
pp. 359
Author(s):  
Jia LI ◽  
Delin XU ◽  
Hai LONG ◽  
Guangbing DENG ◽  
Zhifen PAN ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Wheat Root ◽  
Cyst Nematode ◽  
Nematode Infection ◽  
Cereal Cyst Nematode ◽  
Defense Enzyme

Role of Histamine and Leucotaxin in Function of Cellular Defense Mechanism

1956 ◽  
Vol 184 (2) ◽  
pp. 296-300 ◽  
Author(s):  
László Kátó ◽  
Béla Gözsy
Keyword(s):  
Fluid Flow ◽  
Tissue Damage ◽  
Inflammatory Process ◽  
Defense Mechanism ◽  
Volatile Oils ◽  
Time Intervals ◽  
Cellular Defense ◽  
Intradermal Administration ◽  
Flow Through

Experiments are presented to the effect that in an inflammatory process histamine and leucotaxin appear successively at different and orderly time intervals, thus assuring an increased fluid flow through the capillary wall. Histamine is released not only in the inflammatory process but also by intradermal administration of such substances (volatile oils or their components) which induce neither the triple response of Th. Lewis nor any tissue damage. This could be explained by the fact that in the tissues histamine is ‘present’ but leucotaxin is ‘formed.’

scholarly journals PPAR-γImpairment Alters Peroxisome Functionality in Primary Astrocyte Cell Cultures

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Lorenzo Di Cesare Mannelli ◽  
Matteo Zanardelli ◽  
Laura Micheli ◽  
Carla Ghelardini
Keyword(s):  
Antioxidant Defenses ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Peroxisome Proliferator ◽  
Defense Enzyme ◽  
Primary Astrocyte ◽  
Antioxidant Defense Enzyme ◽  
Rat Astrocytes ◽  
Series Of Experiments ◽  
Peroxisome Proliferator Activated Receptors ◽  
Acyl Coenzyme A

Peroxisomes provide glial cells with protective functions against the harmful effects of H2O2on neurons and peroxisome impairment results in nervous lesions. Agonists of theγ-subtype of the Peroxisome-Proliferator-Activated-Receptors (PPAR) have been proposed as neuroprotective agents in neurodegenerative disorders. Nevertheless, the role of PPAR-γalterations in pathophysiological mechanisms and the relevance of peroxisome functions in the PPAR-γeffects are not yet clear. In a primary cell culture of rat astrocytes, the irreversible PPAR-γantagonist GW9662 concentration-dependently decreased the activity of catalase, the most important antioxidant defense enzyme in peroxisomes. Catalase functionality recovered in a few days and the PPAR-γagonist rosiglitazone promoted reversal of enzymatic damage. The reversible antagonist G3335 reduced both the activity and expression of catalase in a rosiglitazone-prevented manner. G3335 reduced also the glutathione reductase expression, indicating that enzyme involved in glutathione regeneration was compromised. Neither the PPAR-αtarget gene Acyl-Coenzyme-A-oxidase-1 nor the mitochondrial detoxifying enzyme NADH:ubiquinone-oxidoreductase (NDFUS3) was altered by PPAR-γinhibition. In conclusion, PPAR-γinhibition induced impairment of catalase in astrocytes. A general decrease of the antioxidant defenses of the cell suggests that a PPAR-γhypofunction could participate in neurodegenerative mechanisms through peroxisomal damage. This series of experiments could be a useful model for studying compounds able to restore peroxisome functionality.

Autophagy at the crossroads of metabolism and cellular defense

2013 ◽  
Vol 29 (6) ◽  
pp. 588-596 ◽  
Author(s):  
Jakob Begun ◽  
Ramnik J. Xavier
Keyword(s):  
Cellular Defense

A new method of long-term preventive cardioprotection usingLactobacillus

2000 ◽  
Vol 278 (5) ◽  
pp. H1717-H1724 ◽  
Author(s):  
Tatyana Oxman ◽  
Michal Shapira ◽  
Adriana Diver ◽  
Rodica Klein ◽  
Natalie Avazov ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Stress Protein ◽  
Beneficial Effects ◽  
Cellular Defense ◽  
Heat Stress Protein ◽  
Protective Proteins ◽  
Perfused Hearts ◽  
Related Compounds ◽  
Stop Flow

Potential long-term cardioprotection was investigated in an extensive experimental study. Lactobacillus cultivation components (LCC) were administered intravenously in anesthetized rats 1, 7, and 21 days before global ischemia (GI). GI was produced by full stop flow in isolated Langendorff-perfused hearts for 20 min and was followed by reperfusion. Control animals were injected with saline. LCC reduced reperfusion tachyarrhythmia significantly and improved functional recovery of the ischemized rat heart. These beneficial effects were associated with reduction of release of norepinephrine (NE) and prostacyclin at the first minute of reperfusion, activation of myocardial catalase, and overexpression of 70-kDa heat stress protein (HSP-70) at ischemia and reperfusion ( P < 0.05). This cardioprotection was documented up to 21 days after a single injection of LCC. Thus Lactobacillus cultivation components are new nontoxic materials that produce marked long-term cardioprotection against ischemia-reperfusion damage. This effect is attributed to an activation of the cellular defense system, manifested by activation of the antioxidant pathway and by expression of protective proteins. NE is involved in this process, and the data also suggest a role for prostacyclin in this model of cardioprotection. The potential of LCC and related compounds working through similar mechanisms in the prevention and therapy of various ischemic heart syndromes should be explored.

Sign in / Sign up

Export Citation Format

Share Document