Bio-synthesized selenium nanoparticles ameliorate Brain oxidative stress in Parkinson disease rat models

Hashemy, Seyed Isaac; Amiri, Hamed; Joshaghani, Hamidreza; Hosseini, Mahmoud; Hashemy, Seyed Isaac

doi:10.1007/s11011-023-01222-6

Cited by 11 publications

(3 citation statements)

References 47 publications

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“…Moreover, the protective efficacy of SeNPs extends to neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. A shared hallmark of SeNPs across these neurodegenerative conditions is their ability to suppress oxidative stress (Rajeshkumar et al, 2019;Salaramoli et al, 2023).…”

Section: Metallic Nanoparticles Such As Ionps Can Disrupt Iron Homeos...mentioning

confidence: 99%

Implications of environmental nanoparticles on neurodegeneration

Hermosillo‐Abundis,

Méndez‐Rojas,

Arias‐Carrión

2024

J of Neuroscience Research

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The ubiquity of nanoparticles, sourced from both natural environments and human activities, presents critical challenges for public health. While offering significant potential for innovative biomedical applications—especially in enhancing drug transport across the blood–brain barrier—these particles also introduce possible hazards due to inadvertent exposure. This concise review explores the paradoxical nature of nanoparticles, emphasizing their promising applications in healthcare juxtaposed with their potential neurotoxic consequences. Through a detailed examination, we delineate the pathways through which nanoparticles can reach the brain and the subsequent health implications. There is growing evidence of a disturbing association between nanoparticle exposure and the onset of neurodegenerative conditions, highlighting the imperative for comprehensive research and strategic interventions. Gaining a deep understanding of these mechanisms and enacting protective policies are crucial steps toward reducing the health threats of nanoparticles, thereby maximizing their therapeutic advantages.

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Section: Metallic Nanoparticles Such As Ionps Can Disrupt Iron Homeos...mentioning

confidence: 99%

Implications of environmental nanoparticles on neurodegeneration

Hermosillo‐Abundis,

Méndez‐Rojas,

Arias‐Carrión

2024

J of Neuroscience Research

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“…Hence, we inferred that Pb can down-regulate GSH and TAC, up-regulate MDA, and lead to oxidative stress in chicken Ces and Thi. Additionally, Salaramoli et al (2023) demonstrated that Se ameliorated oxidative stress in the brains of rats with Parkinson’s disease by up-regulating TAC and down-regulating MDA [ 18 ]. Se supplement relieved Cd-induced cerebral oxidative stress via increasing GSH and TAC and decreasing MDA in rabbits [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury

Li,

Liang,

Jiang

et al. 2024

Antioxidants

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Lead (Pb), a heavy metal environmental pollutant, poses a threat to the health of humans and birds. Inflammation is one of the most common pathological phenomena in the case of illness and poisoning. However, the underlying mechanisms of inflammation remain unclear. The cerebellum and the thalamus are important parts of the nervous system. To date, there have been no reports of Pb inducing inflammation in animal cerebellums or thalami. Selenium (Se) can relieve Pb poisoning. Therefore, we aimed to explore the mechanism by which Se alleviates Pb toxicity to the cerebellums and thalami of chickens by establishing a chicken Pb or/and Se treatment model. Our results demonstrated that exposure to Pb caused inflammatory damage in cerebellums and thalami, evidenced by the characteristics of inflammation, the decrease in anti-inflammatory factors (interleukin (IL)-2 and interferon-γ (INF-γ)), and the increase in pro-inflammatory factors (IL-4, IL-6, IL-12β, IL-17, and nitric oxide (NO)). Moreover, we found that the IL-2/IL-17–NO pathway took part in Pb-caused inflammatory injury. The above findings were reversed by the supplementation of dietary Se, meaning that Se relieved inflammatory damage caused by Pb via the IL-2/IL-17–NO pathway. In addition, an up-regulated oxidative index malondialdehyde (MDA) and two down-regulated antioxidant indices (glutathione (GSH) and total antioxidant capacity (TAC)) were recorded after the chickens received Pb stimulation, indicating that excess Pb caused an oxidant/antioxidant imbalance and oxidative stress, and the oxidative stress mediated inflammatory damage via the GSH–IL-2 axis. Interestingly, exposure to Pb inhibited four glutathione peroxidase (GPx) family members (GPx1, GPx2, GPx3, and GPx4), three deiodinase (Dio) family members (Dio1, Dio2, and Dio3), and fifteen other selenoproteins (selenophosphate synthetase 2 (SPS2), selenoprotein (Sel)H, SelI, SelK, SelM, SelO, SelP1, SelPb, SelS, SelT, SelU, and selenoprotein (Sep)n1, Sepw1, Sepx1, and Sep15), suggesting that Pb reduced antioxidant capacity and resulted in oxidative stress involving the SPS2–GPx1–GSH pathway. Se supplementation, as expected, reversed the changes mentioned above, indicating that Se supplementation improved antioxidant capacity and mitigated oxidative stress in chickens. For the first time, we discovered that the SPS2–GPx1–GSH–IL-2/IL-17–NO pathway is involved in the complex inflammatory damage mechanism caused by Pb in chickens. In conclusion, this study demonstrated that Se relieved Pb-induced oxidative stress and inflammatory damage via the SPS2–GPx1–GSH–IL-2/IL-17–NO pathway in the chicken nervous system. This study offers novel insights into environmental pollutant-caused animal poisoning and provides a novel theoretical basis for the detoxification effect of Se against oxidative stress and inflammation caused by toxic pollutants.

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“…Also, patients encounter autonomic malfunctions with hypotension, defecation, urinary, and sleep disorders [ 2 ]. PD is identified by losing dopaminergic neurons in the substantia nigra pars compacta (SNpc), deposition and aggregation of alpha-synuclein ( α -Syn) into Lewy bodies, and neurites or oxidative stress [ 3 , 4 ]. Besides, glial neuroinflammatory reactions are contributed to degenerative procedures in PD [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Salivary Biomarkers: Noninvasive Ways for Diagnosis of Parkinson’s Disease

Hashemy

Joshaghani

Hashemy

2023

Neurology Research International

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Finding reliable biomarkers has a crucial role in Parkinson’s disease (PD) assessments. Saliva is a bodily fluid, which might be used as a source of biomarkers for PD. Our article has reviewed several publications on salivary proteins in PD patients and their potential as biomarkers. We find out that α-Syn’s proportion in oligomeric form is higher in PD patients’ saliva, which is potent to use as a biomarker for PD. The salivary concentration of DJ-1 and alpha-amylase is lower in PD patients. Also, substance P level is more moderate in PD patients. Although salivary flow rate is decreased in PD patients, high levels of heme oxygenase and acetylcholinesterase might be used as noninvasive biomarkers. Salivary miRNAs (miR-153, miR-223, miR-874, and miR-145-3p) are novel diagnostic biomarkers that should be given more attention.

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Bio-synthesized selenium nanoparticles ameliorate Brain oxidative stress in Parkinson disease rat models

Cited by 11 publications

References 47 publications

Implications of environmental nanoparticles on neurodegeneration

Implications of environmental nanoparticles on neurodegeneration

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury

Salivary Biomarkers: Noninvasive Ways for Diagnosis of Parkinson’s Disease

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