Protective Effects of Co-administration of Zinc and Selenium Against Streptozotocin-Induced Alzheimer’s Disease: Behavioral, Mitochondrial Oxidative Stress, and GPR39 Expression Alterations in Rats

Farbood, Yaghoob; Sarkaki, Alireza; Mahdavinia, Masoud; Ghadiri, Ata; Teimoori, Ali; Seif, Faezeh; Dehghani, Mohammad Amin; Navabi, Seyedeh Parisa

doi:10.1007/s12640-020-00226-9

Cited by 21 publications

(17 citation statements)

References 45 publications

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“…Co-treatment with zinc and Se significantly decreased mitochondrial dysfunction, ROS levels, and lipid peroxidation levels, while significantly increasing cognitive performance, SOD, glutathione peroxidase, and catalase activity in the mitochondria of the brain in an AD rat model [ 125 ]. In a double-blind, placebo-controlled trial of zinc supplementation for premenstrual syndrome, sixty women (18–30 years) were randomly assigned to receive either 30 mg of zinc gluconate and/or placebo for 12 weeks.…”

Section: Role Of Antioxidants In the Brainmentioning

confidence: 99%

Neuroprotective Effect of Antioxidants in the Brain

Lee

Cha

2020

IJMS

251

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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Section: Role Of Antioxidants In the Brainmentioning

confidence: 99%

Neuroprotective Effect of Antioxidants in the Brain

Lee

Cha

2020

IJMS

251

154

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“…Reduced concentration of selenium as an antioxidant could be associated with AD because of oxidative stress induced by other metals/metalloids (chromium, arsenic, etc.). Experimental studies show a decisive role of selenium in AD pathogenesis via abilities to reduce mitochondrial oxidative stress [ 60 ], to inhibit metal-induced Aβ aggregation [ 33 ] and to reduce Tau hyperphosphorylation [ 61 , 62 ]. Meanwhile, the findings of epidemiological studies are inconsistent.…”

Section: Discussionmentioning

confidence: 99%

Alzheimer’s Disease Association with Metals and Metalloids Concentration in Blood and Urine

Strumylaitė

Kregždytė

Kučikienė

et al. 2022

IJERPH

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As there is some evidence that the risk for Alzheimer’s disease (AD) is partially attributable to environmental exposure to some metals and metalloids, we examined an association between AD and arsenic, chromium, and selenium in 53 AD patients and 217 controls. Urinary arsenic, blood chromium, and selenium were determined by inductively coupled plasma mass spectrometry. Logistic regression models calculating odds ratios (ORs) and 95% confidence intervals (CI) were used to estimate AD association with arsenic, chromium, and selenium. In AD patients, urinary arsenic and blood chromium were significantly higher, while blood selenium was significantly lower compared to controls. Increased blood selenium was related to a significant decrease in the odds of AD after adjustment for risk factors. Blood selenium per 1 kg × 10−9/m3 × 10−4 increment was associated with 1.4 times lower risk of AD (OR = 0.71; 95% CI 0.58–0.87). A significant increase in the odds of AD associated with increased blood chromium was also seen in the adjusted model: the OR per 1 kg × 10−9/m3 × 10−3 chromium increment was 2.39 (95% CI 1.32–4.31). The association of urinary arsenic with the risk of AD was not significant. The data obtained provide evidence that selenium reduces the risk of Alzheimer’s disease, while chromium increases it.

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“…As the zinc content in the body decreases with age, abnormal zinc metabolism may serve as a therapeutic target for AD. In particular, zinc and selenium or iron and zinc have been concomitantly used to treat AD[ 32 , 33 ].…”

Section: Ad and Micronutrientsmentioning

confidence: 99%

Role of micronutrients in Alzheimer's disease: Review of available evidence

Hong-xin¹,

Qian²,

Wu³

et al. 2022

WJCC

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Alzheimer's disease (AD) is one of the most common age-related neurodegenerative disorders that have been studied for more than 100 years. Although an increased level of amyloid precursor protein is considered a key contributor to the development of AD, the exact pathogenic mechanism remains known. Multiple factors are related to AD, such as genetic factors, aging, lifestyle, and nutrients. Both epidemiological and clinical evidence has shown that the levels of micronutrients, such as copper, zinc, and iron, are closely related to the development of AD. In this review, we summarize the roles of eight micronutrients, including copper, zinc, iron, selenium, silicon, manganese, arsenic, and vitamin D in AD based on recently published studies.

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Protective Effects of Co-administration of Zinc and Selenium Against Streptozotocin-Induced Alzheimer’s Disease: Behavioral, Mitochondrial Oxidative Stress, and GPR39 Expression Alterations in Rats

Cited by 21 publications

References 45 publications

Neuroprotective Effect of Antioxidants in the Brain

Neuroprotective Effect of Antioxidants in the Brain

Alzheimer’s Disease Association with Metals and Metalloids Concentration in Blood and Urine

Role of micronutrients in Alzheimer's disease: Review of available evidence

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