Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease

Babušíková, Eva; Evinová, Andrea; Hatok, Jozef; Dobrota, Dušan; Jurečeková, Jana

doi:10.5772/54619

Cited by 4 publications

(4 citation statements)

References 178 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CAT is a critical antioxidant for monitoring H 2 O 2 concentrations in the intracellular space by reducing peroxisomal H 2 O 2 to oxygen and water (Babusikova et al, 2013a,b). Although no studies have examined the impact of human CAT deficiency on the brain in vivo , animal studies have shown that CAT knockout mice demonstrate a slower rate of ATP synthesis in brain mitochondria compared with transgenic mice with CAT overexpression (Schriner et al, 2005).…”

Section: Specific Mechanisms Of Antioxidant Enzymes and Associated Pomentioning

confidence: 99%

“…The cytosolic GST family can be further divided into eight subclasses: Alpha, Kappa, Mu, Pi, Sigma, Theta, Zeta, and Omega (Hayes and Strange, 2000). The Mu class of the human GST gene family (GSTM1) is highly expressed in brain tissue and contains an enzyme deletion polymorphism that contributes to impaired GST function (Babusikova et al, 2013a). GSTM1 is present in two functionally equivalent alleles (A and B) and appears as heterozygous or homozygous (denoted as GSTM1 *1/1 and GSTM1 *0/1), although heterozygosity is rarely examined independently due to the dominant effect of the enzyme deletion (Carlsten et al, 2008).…”

Section: Specific Mechanisms Of Antioxidant Enzymes and Associated Pomentioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

Salminen

Paul

2014

Reviews in the Neurosciences

View full text Add to dashboard Cite

AbstractNormal aging involves a gradual breakdown of physiological processes that leads to a decline in cognitive functions and brain integrity, yet the onset and progression of decline are variable among older individuals. While many biological changes may contribute to this degree of variability, oxidative stress is a key mechanism of the aging process that can cause direct damage to cellular architecture within the brain. Oligodendrocytes are at a high risk for oxidative damage due to their role in myelin maintenance and production and limited repair mechanisms, suggesting that white matter may be particularly vulnerable to oxidative activity. Antioxidant defense enzymes within the brain, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), are crucial for breaking down the harmful end products of oxidative phosphorylation. Previous studies have revealed that allele variations of polymorphisms that encode these antioxidants are associated with abnormalities in SOD, CAT, GPx, and GST activity in the central nervous system. This review will focus on the role of oxidative stress in the aging brain and the impact of decreased antioxidant defense on brain integrity and cognitive function. Directions for future research investigations of antioxidant defense genes will also be discussed.

show abstract

Section: Specific Mechanisms Of Antioxidant Enzymes and Associated Pomentioning

confidence: 99%

Section: Specific Mechanisms Of Antioxidant Enzymes and Associated Pomentioning

confidence: 99%

Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

Salminen

Paul

2014

Reviews in the Neurosciences

View full text Add to dashboard Cite

show abstract

“…Catalase is a critical antioxidant in the intracellular space which acts by reducing peroxisomal H 2 O 2 to oxygen and water. 25 Catalase activity in both cerebellum and hippocampus decreased with an increase in Al dose. In the case of catalase in hippocampus we observed significant reduction even in Al 50 dose in 8-week duration, clearly indicating the depletion of its activity even in low doses when exposed to a longer duration of Al exposure.…”

Section: Discussionmentioning

confidence: 96%

Pro-Oxidant and Antioxidant Activity in Female Rat Cerebellum and Hippocampus on Exposure to Aluminium

Bandi,

Nayak,

Mallipeddi

et al. 2023

Int J. Pharm. Investigation

View full text Add to dashboard Cite

Background: The brain is highly susceptible to Aluminium's (Al) toxic impact due to its elevated lipid content and oxygen utilization but, relatively scanty levels of antioxidants. Al is known for its strong pro-oxidant activity. Hence oxidative stress in the brain is a likely outcome of Al toxicity. Previous studies report sensory, motor and cognitive deficits in animals exposed to various Al compounds. Hence, this study was undertaken to find how dose, and time span of aluminium exposure influence the pro-oxidant activity and antioxidant handling capacity in female Wistar rats' cerebellum and hippocampus. Materials and Methods: Two groups of female Wistar rats were given four different aluminium chloride oral doses of 0, 50, 100, 200 mg/Kg body weight daily for a time span of four and eight weeks. Oxidative level was assessed by estimating GSH, LPO, SOD, Catalase, GPx and GR in cerebellum and hippocampus of rat brain. Data was analysed by 2-way ANOVA and Bonferroni 't' test was used for multiple group comparisons. Results: Al exposure in female rats resulted in increased lipid peroxidation, while antioxidants GSH, SOD, catalase, GPx and GR were depleted in cerebellum and hippocampus. However, these changes were predominantly significant only in aluminium doses of 100 and 200 mg/Kg in both 4 and 8weeks studies. But, GPx in the cerebellum and catalase in hippocampus showed a crucial reduction even at 50 mg/Kg dose on eight-week exposure. Conclusion: Aluminium has enhanced the synthesis of Reactive Oxygen Species (ROS) in rat cerebellum and hippocampus, as noted by the increase in lipid peroxidation which was not balanced by the elevated synthesis of antioxidants. In addition, aluminium at higher doses of 100mg/Kg dose and more had a significant negative impact on the antioxidant protective system. Therefore, it is vital to minimize our aluminium exposure from different sources in our everyday lives.

show abstract

“…In normal cells, ROS is now established to play key signaling roles in cell differentiation, autophagy and immune responses (Sena and Chandel, 2012; Ray et al, 2012). However, accumulation of intracellular ROS is potentially harmful to normal cells, causing oxidation of nucleic acids, proteins, and lipids, and can lead to oxidative stress (Cooke et al, 2003; Babusikova et al, 2013; Bernard et al, 2012; Sawada and Carlson, 1987). The deleterious effects of ROS have been associated with numerous human pathologies such as aging, cardiovascular diseases, neurodegenerative diseases and cancer (Brieger et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses

Choi

Harhaj²

2014

Front. Biol.

View full text Add to dashboard Cite

Between 15–20% of human cancers are associated with infection by oncogenic viruses. Oncogenic viruses, including HPV, HBV, HCV and HTLV-1, target mitochondria to influence cell proliferation and survival. Oncogenic viral gene products also trigger the production of reactive oxygen species which can elicit oxidative DNA damage and potentiate oncogenic host signaling pathways. Viral oncogenes may also subvert mitochondria quality control mechanisms such as mitophagy and metabolic adaptation pathways to promote virus replication. Here, we will review recent progress on viral regulation of mitophagy and metabolic adaptation and their roles in viral oncogenesis.

show abstract

Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease

Cited by 4 publications

References 178 publications

Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

Pro-Oxidant and Antioxidant Activity in Female Rat Cerebellum and Hippocampus on Exposure to Aluminium

Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses

Contact Info

Product

Resources

About