Endogenous antioxidant defence system in rat liver following mercury chloride oral intoxication

2005 ◽  
Vol 19 (3) ◽  
pp. 154-161 ◽  
Author(s):  
Inmaculada Bando ◽  
María Isabel Sánchez Reus ◽  
David Andrés ◽  
María Cascales
Keyword(s):  
Rat Liver ◽  
Mercury Chloride ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System ◽  
Endogenous Antioxidant ◽  
Endogenous Antioxidant Defence

Anti-carcinogenic action of curcumin by activation of antioxidant defence system and inhibition of NF-κB signalling in lymphoma-bearing mice

2011 ◽  
Vol 32 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Laxmidhar Das ◽  
Manjula Vinayak
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Antioxidant Enzymes ◽  
Morphological Changes ◽  
Nuclear Factor Κb ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System ◽  
Endogenous Antioxidant ◽  
Endogenous Antioxidant Defence

NF-κB (nuclear factor κB) plays a significant role in inflammation, immunity, cell proliferation, apoptosis and malignancy. ROS (reactive oxygen species) are among the most important regulating factors of NF-κB. Intracellular ROS are mainly regulated by an endogenous antioxidant defence system. Any disruption of redox balance leads to oxidative stress, which causes a number of pathological conditions including inflammation and malignancy. Increased metabolic activity in cancerous cells leads to oxidative stress, which is further enhanced due to depletion of the endogenous antioxidant defence system. However, the activation and signalling of NF-κB are reported to be inhibited by overexpression and induced activity of antioxidant enzymes. Therefore the present study focuses on the correlation between the endogenous antioxidant defence system, ROS and NF-κB activation during lymphoma growth in mice. The study highlights the anti-carcinogenic role of curcumin by modulation of NF-κB activation and oxidative stress via the endogenous antioxidant defence system. Oxidative stress was monitored by lipid peroxidation, protein carbonylation and antioxidant enzyme activity. NF-κB-mediated signalling was tested by DNA-binding activity. The results reflect that intracellular production of H2O2 in oxidative tumour micro-environment regulates NF-κB activation. Curcumin inhibits oxidative state in the liver of lymphoma-bearing mice by enhancing the transcription and activities of antioxidant enzymes, which in turn modulate activation of NF-κB, leading to a decrease in lymphoma growth. Morphological changes as well as cell proliferation and cell survival assays confirmed reduced lymphoma growth. Thus curcumin contributes to cancer prevention by disrupting the vicious cycle of constant ROS production, responsible for a high oxidative micro-environment for tumour growth.

Effect of Fish Oil and Coconut Oil on Antioxidant Defence System and Lipid Peroxidation in Rat Liver

1991 ◽  
Vol 12 (1) ◽  
pp. 147-152 ◽  
Author(s):  
Massimo D'aquino ◽  
Paola Corcos Benedetti ◽  
Maurizio Di Felice ◽  
Vincenzo Gentili ◽  
Gianni Tomassi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fish Oil ◽  
Rat Liver ◽  
Coconut Oil ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System

scholarly journals Downregulation of FeSOD-A expression in Leishmania infantum alters trivalent antimony and miltefosine susceptibility

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ana Maria Murta Santi ◽  
Paula Alves Silva ◽  
Isabella Fernandes Martins Santos ◽  
Silvane Maria Fonseca Murta
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Leishmania Infantum ◽  
Transcript Level ◽  
Drug Susceptibility ◽  
Central Component ◽  
Multiplication Rate ◽  
Antioxidant Defence ◽  
Defence System ◽  
Antioxidant Defence System

Abstract Background Superoxide dismutase (SOD), a central component of the antioxidant defence system of most organisms, removes excess superoxide anions by converting them to oxygen and hydrogen peroxide. As iron (Fe) SOD is absent in the human host, this enzyme is a promising molecular target for drug development against trypanosomatids. Results We obtained Leishmania infantum mutant clones with lower FeSOD-A expression and investigated their phenotypes. Our attempts to delete this enzyme-coding gene using three different methodologies (conventional allelic replacement or two different CRISPR/methods) failed, as FeSOD-A gene copies were probably retained by aneuploidy or gene amplification. Promastigote forms of WT and mutant parasites were used in quantitative reverse-transcription polymerase chain reaction (RT-qPCR) and western blot analyses, and these parasite forms were also used to assess drug susceptibility. RT-qPCR and western blot analyses revealed that FeSOD-A transcript and protein levels were lower in FeSOD-A−/−/+L. infantum mutant clones than in the wild-type (WT) parasite. The decrease in FeSOD-A expression in L. infantum did not interfere with the parasite growth or susceptibility to amphotericin B. Surprisingly, FeSOD-A−/−/+L. infantum mutant clones were 1.5- to 2.0-fold more resistant to trivalent antimony and 2.4- to 2.7-fold more resistant to miltefosine. To investigate whether the decrease in FeSOD-A expression was compensated by other enzymes, the transcript levels of five FeSODs and six enzymes from the antioxidant defence system were assessed by RT-qPCR. The transcript level of the enzyme ascorbate peroxidase increased in both the FeSOD-A−/−/+ mutants tested. The FeSOD-A−/−/+ mutant parasites were 1.4- to 1.75-fold less tolerant to oxidative stress generated by menadione. Infection analysis using THP-1 macrophages showed that 72 h post-infection, the number of infected macrophages and their intracellular multiplication rate were lower in the FeSOD-A−/−/+ mutant clones than in the WT parasite. Conclusions The unsuccessful attempts to delete FeSOD-A suggest that this gene is essential in L. infantum. This enzyme plays an important role in the defence against oxidative stress and infectivity in THP-1 macrophages. FeSOD-A-deficient L. infantum parasites deregulate their metabolic pathways related to antimony and miltefosine resistance. Graphic Abstract

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