Selenium reduces bradykinesia and DNA damage in a rat model of Parkinson's disease

Ellwanger, Joel Henrique; Molz, Patrí­cia; Dallemole, Danieli Rosane; Santos, Ariana Pereira Dos; Müller, Talise E.; Cappelletti, Lucas; Silva, Manoela Gonçalves da; Franke, Silvia Isabel Rech; Prá, Daniel; Henriques, João Antônio Pêgas

doi:10.1016/j.nut.2014.07.004

Cited by 44 publications

(26 citation statements)

References 45 publications

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“…Previous studies found reduced selenium levels in PD patients (Shahar et al 2010). In addition, selenium reduces bradykinesia, a well-described symptom of PD, in rats (Ellwanger et al 2015), suggesting that higher selenium levels would be beneficial for PD patients. A GWAS hit for PD (Do et al 2011;International Parkinson Disease Genomics Consortium 2011) was an eQTL for LAMP3, where the reference/PD-risk allele led to increased expression of LAMP3 (The GTEx Consortium 2015).…”

Section: Wwwgenomeorgmentioning

confidence: 99%

High-throughput allele-specific expression across 250 environmental conditions

et al. 2016

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Gene-by-environment (GxE) interactions determine common disease risk factors and biomedically relevant complex traits. However, quantifying how the environment modulates genetic effects on human quantitative phenotypes presents unique challenges. Environmental covariates are complex and difficult to measure and control at the organismal level, as found in GWAS and epidemiological studies. An alternative approach focuses on the cellular environment using in vitro treatments as a proxy for the organismal environment. These cellular environments simplify the organism-level environmental exposures to provide a tractable influence on subcellular phenotypes, such as gene expression. Expression quantitative trait loci (eQTL) mapping studies identified GxE interactions in response to drug treatment and pathogen exposure. However, eQTL mapping approaches are infeasible for large-scale analysis of multiple cellular environments. Recently, allele-specific expression (ASE) analysis emerged as a powerful tool to identify GxE interactions in gene expression patterns by exploiting naturally occurring environmental exposures. Here we characterized genetic effects on the transcriptional response to 50 treatments in five cell types. We discovered 1455 genes with ASE (FDR < 10%) and 215 genes with GxE interactions. We demonstrated a major role for GxE interactions in complex traits. Genes with a transcriptional response to environmental perturbations showed sevenfold higher odds of being found in GWAS. Additionally, 105 genes that indicated GxE interactions (49%) were identified by GWAS as associated with complex traits. Examples include GIPR-caffeine interaction and obesity and include LAMP3-selenium interaction and Parkinson disease. Our results demonstrate that comprehensive catalogs of GxE interactions are indispensable to thoroughly annotate genes and bridge epidemiological and genomewide association studies.

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Section: Wwwgenomeorgmentioning

confidence: 99%

High-throughput allele-specific expression across 250 environmental conditions

et al. 2016

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“…Selenite administration in a rat AD model also showed attenuation of cognitive deficits, oxidative damage and morphological changes in the hippocampus and cerebral cortex [ 103 ]. In a paraquat induced PD model, bradykinesia and DNA damage reduction were observed by supplementing Se with selenite in drinking water [ 104 ]. Alterations of Se homeostasis in the HD model have been observed and a beneficial effect of selenite supplementation in mice expressing mutant huntingtin has been reported.…”

Section: Role Of Antioxidants In the Brainmentioning

confidence: 99%

Neuroprotective Effect of Antioxidants in the Brain

Lee

Cha

2020

IJMS

283

154

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The brain is vulnerable to excessive oxidative insults because of its abundant lipid content, high energy requirements, and weak antioxidant capacity. Reactive oxygen species (ROS) increase susceptibility to neuronal damage and functional deficits, via oxidative changes in the brain in neurodegenerative diseases. Overabundance and abnormal levels of ROS and/or overload of metals are regulated by cellular defense mechanisms, intracellular signaling, and physiological functions of antioxidants in the brain. Single and/or complex antioxidant compounds targeting oxidative stress, redox metals, and neuronal cell death have been evaluated in multiple preclinical and clinical trials as a complementary therapeutic strategy for combating oxidative stress associated with neurodegenerative diseases. Herein, we present a general analysis and overview of various antioxidants and suggest potential courses of antioxidant treatments for the neuroprotection of the brain from oxidative injury. This review focuses on enzymatic and non-enzymatic antioxidant mechanisms in the brain and examines the relative advantages and methodological concerns when assessing antioxidant compounds for the treatment of neurodegenerative disorders.

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“…In addition, the comet assay with hippocampal cells is a well-established methodology in our group (Molz et al 2016). The assay was performed according to Singh et al (1988), with adaptations detailed described in previous studies published by our group (Ellwanger et al 2015, Molz et al 2016, Franke et al 2017. Briefly, one hundred nucleoids ("comets") per sample were randomly selected and analyzed using a conventional microscope.…”

Section: Dna Damage Evaluationmentioning

confidence: 99%

Influence of hesperidin and vitamin C on glycemic parameters, lipid profile, and DNA damage in rats treated with sucrose overload

Franke

Molz

Mai

et al. 2018

An. Acad. Bras. Ciênc.

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We evaluated the influence of hesperidin and vitamin C (VitC) on glycemic parameters, lipid profile, and DNA damage in male Wistar rats treated with sucrose overload. Rats were divided into six experimental groups: I-water control; II-sucrose control; III-hesperidin control; IV-VitC control; V-co-treatment of sucrose plus hesperidin; VI-co-treatment of sucrose plus VitC. We measured the levels of triglycerides, total cholesterol, HDL-c, LDL-c, fasting glucose, and glycated hemoglobin (A1C). DNA damage was evaluated in blood and brain cells using the comet assay and the micronucleus test was used to evaluate chromosomal damages in the rat bone marrow. Co-treatment with VitC, but not with hesperidin, normalized the serum glucose. No effect of co-treatments was observed on A1C. The co-treatment with VitC or hesperidin did not influence the lipid profile (p>0.05). Rats co-treated with hesperidin had a significantly lower DNA damage level in blood (p<0.05) and brain (p<0.05). Rats treated with VitC only, but not those co-treated with VitC plus sucrose, had significantly higher DNA damage in brain (p<0.05). No significant differences were observed in the results of micronucleus test (p>0.05). Hesperidin and VitC showed different effects on sucrose and DNA damage levels. While VitC lowered the serum glucose, hesperidin reduced the DNA damage.

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Selenium reduces bradykinesia and DNA damage in a rat model of Parkinson's disease

Cited by 44 publications

References 45 publications

High-throughput allele-specific expression across 250 environmental conditions

High-throughput allele-specific expression across 250 environmental conditions

Neuroprotective Effect of Antioxidants in the Brain

Influence of hesperidin and vitamin C on glycemic parameters, lipid profile, and DNA damage in rats treated with sucrose overload

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