In vitro studies on radiation induced membrane oxidative damage in apoptotic death of mouse thymocytes

2003 ◽  
Vol 1 (1) ◽  
pp. 113 ◽  
Author(s):  
B.N. Pandey ◽  
K.P. Mishra
Keyword(s):  
Oxidative Damage ◽  
In Vitro Studies ◽  
Induced Membrane ◽  
Apoptotic Death ◽  
Radiation Induced

scholarly journals Protein damage, ageing and age-related diseases

Open Biology ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 180249 ◽  
Author(s):  
Anita Krisko ◽  
Miroslav Radman
Keyword(s):  
Oxidative Damage ◽  
Protein Damage ◽  
Death Studies ◽  
Root Cause ◽  
Age Related ◽  
Oxidative Protein Damage ◽  
Gompertz Law ◽  
Radiation Induced ◽  
Folded Proteins

Ageing is considered as a snowballing phenotype of the accumulation of damaged dysfunctional or toxic proteins and silent mutations (polymorphisms) that sensitize relevant proteins to oxidative damage as inborn predispositions to age-related diseases. Ageing is not a disease, but it causes (or shares common cause with) age-related diseases as suggested by similar slopes of age-related increase in the incidence of diseases and death. Studies of robust and more standard species revealed that dysfunctional oxidatively damaged proteins are the root cause of radiation-induced morbidity and mortality. Oxidized proteins accumulate with age and cause reversible ageing-like phenotypes with some irreversible consequences (e.g. mutations). Here, we observe in yeast that aggregation rate of damaged proteins follows the Gompertz law of mortality and review arguments for a causal relationship between oxidative protein damage, ageing and disease. Aerobes evolved proteomes remarkably resistant to oxidative damage, but imperfectly folded proteins become sensitive to oxidation. We show that α-synuclein mutations that predispose to early-onset Parkinson's disease bestow an increased intrinsic sensitivity of α-synuclein to in vitro oxidation. Considering how initially silent protein polymorphism becomes phenotypic while causing age-related diseases and how protein damage leads to genome alterations inspires a vision of predictive diagnostic, prognostic, prevention and treatment of degenerative diseases.

The conjugation of Cu/Zn superoxide dismutase (SOD) to O-(2-hydroxyl) propyl-3-trimethyl ammonium chitosan chloride (O-HTCC) enhances its therapeutic potential against radiation-induced oxidative damage

2016 ◽  
Vol 7 (9) ◽  
pp. 1826-1835 ◽  
Author(s):  
Linghua Xu ◽  
Xiaohu Ji ◽  
Nan Zhao ◽  
Chunxia Song ◽  
Fengshan Wang ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Therapeutic Potential ◽  
Enzyme Conjugate ◽  
Radiation Induced

A novel polymer–enzyme conjugate, O-HTCC–SOD, was prepared to improve the therapeutic potential of SOD in vitro and in vivo.

Astrocyte phenotype and prevention against oxidative damage in neurotoxicity

2000 ◽  
Vol 19 (11) ◽  
pp. 641-649 ◽  
Author(s):  
V W Pentreath ◽  
N D Slamon
Keyword(s):  
Oxidative Damage ◽  
Nervous Tissue ◽  
In Vitro Studies ◽  
Toxic Chemicals ◽  
Protective Systems

Astrocytes possess a potent array of protective systems. These are chiefly targeted against oxidised products and radicals, which are frequently present in increased amounts following exposure of nervous tissue to a range of toxic insults. Following exposure to the toxic chemicals astrocytes commonly respond by alteration in phenotype with upregu-lation of a large number of molecules, including those controlling the protective systems. This article summarizes evidence, largely obtained from in vitro studies, which supports the concept that some of the changes in astrocyte phenotype are associated with increased protection against the cytotoxicity caused by the oxidative damage that results from exposure to range of neurotoxicants.

In vitro - studies with antler bone cells: Structure forming capacity, osteocalcin production and influence of sex steroids

2006 ◽  
Vol 15 (04) ◽  
pp. 245-257 ◽  
Author(s):  
H. J. Rolf ◽  
K. G. Wiese ◽  
H. Siggelkow ◽  
H. Schliephake ◽  
G. A. Bubernik
Keyword(s):  
Sex Steroids ◽  
Bone Cells ◽  
In Vitro Studies ◽  
Osteocalcin Production

In Vitro Studies on the Mechanism of the Antifibrino-lytic Action of E-Aminocaproic Acid (EACA)

1968 ◽  
Vol 19 (03/04) ◽  
pp. 584-592 ◽  
Author(s):  
Hanna Lukasiewicz ◽  
S Niewiarowski
Keyword(s):  
Aminocaproic Acid ◽  
Test Tube ◽  
In Vitro Studies ◽  
Lytic Action ◽  
Human Plasminogen ◽  
Experimental Findings ◽  
Fibrin Clots

Summary and Conclusion1. It has been found that EACA does not inhibit activation of human plasminogen into plasmin by SK and UK in a concentration of 5 × 10–2 M. The activation of bovine plasminogen by SK and UK is inhibited by this concentration of EACA but not by a lower one.2. EACA in concentrations of 1,5 × 10–1 – 10–4 M does not inhibit casein proteolysis by plasmin. The proteolysis of fibrinogen and fibrin measured by the release of TCA soluble tyrosine is inhibited by EACA in concentrations of 1,5 × 10–1 – 10–2 M.3. The lysis of non-stabilized clots by plasmin measured in a test tube was inhibited by an EACA concentration of 5 × 10–3 – 5 × 10–4 M. The lysis of stabilized clots by plasmin was inhibited by an EACA concentration of 10–5 M.4. On the basis of experimental findings and data given in literature the authors postulate that the mechanism of the antifibrinolytic effects of EACA consists mainly in a modification of plasmin action on fibrin. These effects are dependent on the structure of the fibrin clots.

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