scholarly journals Endogenous antioxidant defenses in malaria comorbidly occurring with typhoid

2012 ◽  
Vol 2 (4) ◽  
pp. 6-11
Author(s):  
O. Ademuyiwa ◽  
D.A. Ojo ◽  
R.N. Ugbaja ◽  
S.O. Rotimi
Keyword(s):  
Antioxidant Defenses ◽  
Endogenous Antioxidant

scholarly journals Enantioselective Modulatory Effects of Naringenin  Enantiomers on the Expression Levels of miR‐17‐3p  Involved in Endogenous Antioxidant Defenses

Nutrients ◽  
2017 ◽  
Vol 9 (3) ◽  
pp. 215 ◽  
Author(s):  
Valeria Curti ◽  
Arianna Di Lorenzo ◽  
Daniela Rossi ◽  
Emanuela Martino ◽  
Enrica Capelli ◽  
...  
Keyword(s):  
Antioxidant Defenses ◽  
Expression Levels ◽  
Endogenous Antioxidant

Endogenous antioxidant defenses in neonates

1986 ◽  
Vol 2 (4) ◽  
pp. 295-298 ◽  
Author(s):  
Warren Rosenfeld ◽  
Luzminda Concepcion
Keyword(s):  
Antioxidant Defenses ◽  
Endogenous Antioxidant

Antioxidants for human health

2020 ◽  
pp. 22-26
Author(s):  
Biswaranjan Paital ◽  
Keyword(s):  
Free Radicals ◽  
Human Health ◽  
Health Management ◽  
Antioxidant Defenses ◽  
Superoxide Dismutases ◽  
Cellular Architecture ◽  
Vitamins E And C ◽  
Experimental Approaches ◽  
Endogenous Antioxidant ◽  
Ascorbic Acids

Antioxidants are chemical or biochemical substances that are capable to prevent or slow damages occurred to cells caused by free radicals. Free radicals are the chemical entities that are produced due to sharing of unpaired electrons and are with free existence but unstable in nature. Organism’s body produces free radicals as a reaction to environmental and other internal and external stressors. If not neutralized, free radicals can damage cellular architecture by oxidizing all bio-molecules. They are neutralized by antioxidants which are chemicals or biological in origin. Therefore, free radicals and antioxidants are simultaneously and widely discussed in the clinical and nutritional literature. Cellular or endogenous antioxidant defenses includes enzymes (superoxide dismutases, H2O2-removing enzymes such as catalase, and peroxidasses), and non-enzymes such as vitamin C (ascorbic acids, vitamin E and reduced glutathione. Diet-derived antioxidants are important in maintaining health. Many dietary compounds have been suggested to be important antioxidants: Therefore recent interest on dietary vitamins E and C, carotenoids and plant pigments, plant phenolics, especially flavonoids are growing to mauanitn human health. Experimental approaches to the optimization of antioxidant nutrient intake are already known and must be adapted for health management.

Liposome-mediated augmentation of antioxidant defenses in fetal rat pneumocytes

1990 ◽  
Vol 258 (4) ◽  
pp. L165-L172 ◽  
Author(s):  
A. K. Tanswell ◽  
D. M. Olson ◽  
B. A. Freeman
Keyword(s):  
Dna Synthesis ◽  
Prostaglandin Synthesis ◽  
Antioxidant Defenses ◽  
Fetal Cells ◽  
Mediated Effects ◽  
Lactate Dehydrogenase Release ◽  
Low Concentrations ◽  
Inhibit Prostaglandin Synthesis ◽  
Fetal Rat ◽  
Endogenous Antioxidant

Cultured pneumocytes, prepared from fetal rat lung, are growth inhibited and have increased lactate dehydrogenase release and prostaglandin synthesis in response to 50 and 95% O2 exposure. The uptake of cationic liposomes by these fetal cells is more rapid and extensive than is the case with cultured adult pneumocytes. Protection of fetal pneumocytes against the cytotoxic effects of 50 or 95% O2 by liposome-entrapped antioxidant enzymes requires a liposome phospholipid concentration of only 1 nmol/cm2, compared with 45 nmol/cm2 for adult cells, which is a cytotoxic phospholipid concentration for the fetal cells. Despite this capacity of low concentrations of liposomes containing superoxide dismutase and catalase to increase endogenous antioxidant enzyme content, and to protect against cell death, such treatment does not attenuate O2-mediated alterations of cell growth or prostaglandin release. Inhibition of pneumocyte DNA synthesis, by elevated O2 concentrations, cannot be attributed to an autocrine effect of enhanced prostaglandin synthesis, because the addition of 50 microM ibuprofen to inhibit prostaglandin synthesis does not prevent O2-mediated effects on DNA synthesis.

scholarly journals MnTE-2-PyP, a manganese porphyrin, reduces cytotoxicity caused by irradiation in a diabetic environment through the induction of endogenous antioxidant defenses

Redox Biology ◽  
2020 ◽  
Vol 34 ◽  
pp. 101542
Author(s):  
Arpita Chatterjee ◽  
Elizabeth A. Kosmacek ◽  
Shashank Shrishrimal ◽  
J. Tyson McDonald ◽  
Rebecca E. Oberley-Deegan
Keyword(s):  
Antioxidant Defenses ◽  
Manganese Porphyrin ◽  
Endogenous Antioxidant

scholarly journals Induction of Copper-Zinc Superoxide Dismutase in Gerbil Hippocampus after Ischemia

1993 ◽  
Vol 13 (1) ◽  
pp. 135-144 ◽  
Author(s):  
Tomohiro Matsuyama ◽  
Hisamasa Michishita ◽  
Hitoshi Nakamura ◽  
Masato Tsuchiyama ◽  
Souichiro Shimizu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
In Situ Hybridization ◽  
Control Level ◽  
Antioxidant Defenses ◽  
Hybridization Technique ◽  
Copper Zinc Superoxide Dismutase ◽  
Pyramidal Layer ◽  
Endogenous Antioxidant

To assess the role of Cu-Zn superoxide dismutase (CuZnSOD) in regulating cellular antioxidant defenses, we studied the induction of CuZnSOD mRNA by an in situ hybridization technique and of CuZnSOD protein by an immunocytochemical method in the gerbil hippocampus following 5 min of transient global ischemia. For hybridization, we synthesized 48-mer oligonucleotide (base 465–512) complementary to rat CuZnSOD mRNA. Northern blot analysis showed hybridization to a single band of molecular weight 0.65 kb. After 5 min of ischemia, the signal became stronger at 3 and 24 h and returned to the control level 3 days later. In situ hybridization histochemistry revealed an increase in labeling throughout the hippocampus, especially in the granular layer 3 h following ischemia. The increase was prolonged only in the CA1 pyramidal layer after 24 h and was eliminated within 3 days or later. Conversely, analysis by Western blotting revealed that the insult produced few effects on the induction of CuZnSOD protein. Immunocytochemistry for CuZnSOD revealed a reduced immunostaining in the CA1 pyramidal layer at 24 h of recirculation when the persistent expression of CuZnSOD mRNA was shown in the same area. Our findings suggest that the expression of endogenous CuZnSOD is temporarily stimulated by an ischemic insult without increasing the protein level. The prolonged increase in mRNA and the decrease in the protein of CuZnSOD in the CA, neurons seem to imply an important role of the endogenous antioxidant enzyme that protects against the detrimental effects of superoxide radicals on delayed neuronal death.

scholarly journals The Antioxidant 3H-1,2-Dithiole-3-Thione Potentiates Advanced Glycation End-Product-Induced Oxidative Stress in SH-SY5Y Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Robert Pazdro ◽  
John R. Burgess
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Antioxidant Defenses ◽  
Chemical Induction ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
Ros Formation ◽  
Endogenous Antioxidant ◽  
Neurite Degeneration

Oxidative stress is implicated as a major factor in the development of diabetes complications and is caused in part by advanced glycation end products (AGEs). AGEs ligate to the receptor for AGEs (RAGE), promoting protein kinase C (PKC)-dependent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and superoxide radical generation. While scavenging antioxidants are protective against AGEs, it is unknown if induction of endogenous antioxidant defenses has the same effect. In this study, we confirmed that the compound 3H-1,2-dithiole-3-thione (D3T) increases reduced-state glutathione (GSH) concentrations and NADPH:quinone oxidoreductase 1 (NQO1) activity in SH-SY5Y cells and provides protection against H2O2. Surprisingly, D3T potentiated oxidative damage caused by AGEs. In comparison to vehicle controls, D3T caused greater AGE-induced cytotoxicity and depletion of intracellular GSH levels while offering no protection against neurite degeneration or protein carbonylation. D3T potentiated AGE-induced reactive oxygen species (ROS) formation, an effect abrogated by inhibitors of PKC and NADPH oxidase. This study suggests that chemical induction of endogenous antioxidant defenses requires further examination in models of diabetes.

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