Clinical Significance of Serum Zinc Levels in Cerebral Ischemia

Bhatt, Archit; Farooq, Muhammad Umar; Enduri, S.; Pillainayagam, Clement; Naravetla, Bharath; Razak, Anmar; Safdar, Adnan; Hussain, Syed; Kassab, Mounzer; Majid, Arshad

doi:10.4061/2010/245715

Cited by 18 publications

(17 citation statements)

References 25 publications

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“…Disturbed neurogenesis and elevated apoptosis of neuronal cells, which can result in defects in learning and memory, were described during Zn deficiency, as was shown in animals fed on a Zn-deficient diet. Retrospective studies on stroke patients also suggest a clinical significance for serum Zn deficiency (229)(230)(231)(232)(233)(234)(235) . The increase in neuronal apoptosis might involve mitochondrial p53 as well as p53-dependent caspase-mediated mechanisms as shown in vitro (236) .…”

Section: Zinc Deficiency As Pre-requisite To Virus-induced Neuronal Damage and Loss In Smell And Tastementioning

confidence: 99%

Zinc deficiency as a possible risk factor for increased susceptibility and severe progression of Corona Virus Disease 19

et al. 2021

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The importance of zinc for human health becomes obvious during zinc deficiency. Even mild insufficiencies of zinc cause alterations in haematopoiesis and immune functions, resulting in a pro-inflammatory phenotype and a disturbed redox metabolism. Although immune system malfunction is the most obvious effect, the functions of several tissue cell types are disturbed if zinc supply is limiting. Adhesion molecules and tight junction proteins decrease while cell death increases, generating barrier dysfunction and possibly organ failure. Taken together, zinc deficiency both weakens the resistance of the human body towards pathogens and at the same time increases the danger of an overactive immune response that may cause tissue damage. The case numbers of COVID-19 are still increasing, which is causing enormous problems for health systems and economies. There is an urgent need to reduce both the number of severe cases and the resulting deaths. While therapeutic options are still under investigation,and first vaccines have been approved, cost-effective ways to reduce the likelihood of or even prevent infection, and the transition from mild symptoms to more serious detrimental disease, are highly desirable. Nutritional supplementation might be an effective option to achieve these aims. In this review, we discuss known zinc deficiency effects in the context of an infection with SARS-CoV-2 and its currently known pathogenic mechanisms and elaborate on how severe pre-existing zinc deficiency may pre-dispose patients to a severe progression of COVID-19. First published clinical data on the association of zinc homeostasis with COVID-19 and registered studies in progress are listed.

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Section: Zinc Deficiency As Pre-requisite To Virus-induced Neuronal Damage and Loss In Smell And Tastementioning

confidence: 99%

Zinc deficiency as a possible risk factor for increased susceptibility and severe progression of Corona Virus Disease 19

et al. 2021

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“…In this study, lower levels of zinc were associated with increased stroke severity. Additionally, decreased zinc status was associated with poor functional status at discharge, independent of other confounding variables such as age, sex, NIH Stroke Scale score at admission, and other potential comorbidities including hypertension, diabetes, atrial fibrillation, or cognitive heart failure [76]. …”

Section: Zinc and Disorders Of The Central Nervous Systemmentioning

confidence: 99%

Zinc in the central nervous system: From molecules to behavior

2012

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The trace metal zinc is a biofactor that plays essential roles in the central nervous system across the lifespan from early neonatal brain development through the maintenance of brain function in adults. At the molecular level, zinc regulates gene expression through transcription factor activity and is responsible for the activity of dozens of key enzymes in neuronal metabolism. At the cellular level, zinc is a modulator of synaptic activity and neuronal plasticity in both development and adulthood. Given these key roles, it is not surprising that alterations in brain zinc status have been implicated in a wide array of neurological disorders including impaired brain development, neurodegenerative disorders such as Alzheimer’s disease, and mood disorders including depression. Zinc has also been implicated in neuronal damage associated with traumatic brain injury, stroke, and seizure. Understanding the mechanisms that control brain zinc homeostasis is thus critical to the development of preventive and treatment strategies for these and other neurological disorders.

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“…Zinc plays a dual role in the cerebral hypoxia-ischemia depending on its concentration in the cerebral stroke area; this concentration is known to be determined by zinc serum levels [ 1 ]. Accordingly, low serum levels of zinc have long been considered as a risk factor for stroke [ 2 ]. In contrast, the input of low concentration of zinc chloride (ZnCl 2 ) or zinc protoporphyrin (ZnPP) reduces the size of postischemic brain damage [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia‐Ischemia

Tomás-Sanchez

Blanco-Álvarez

Martínez‐Fong

et al. 2018

Oxidative Medicine and Cellular Longevity

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In the cerebral hypoxia-ischemia rat model, the prophylactic administration of zinc can cause either cytotoxicity or preconditioning effect, whereas the therapeutic administration of selenium decreases the ischemic damage. Herein, we aimed to explore whether supplementation of low doses of prophylactic zinc and therapeutic selenium could protect from a transient hypoxic-ischemic event. We administrated zinc (0.2 mg/kg of body weight; ip) daily for 14 days before a 10 min common carotid artery occlusion (CCAO). After CCAO, we administrated sodium selenite (6 μg/kg of body weight; ip) daily for 7 days. In the temporoparietal cerebral cortex, we determined nitrites by the Griess method and lipid peroxidation by the Gerard-Monnier assay. qPCR was used to measure mRNA of nitric oxide synthases, antioxidant enzymes, chemokines, and their receptors. We measured the enzymatic activity of SOD and GPx and protein levels of chemokines and their receptors by ELISA. We evaluated long-term memory using the Morris-Water maze test. Our results showed that prophylactic administration of zinc caused a preconditioning effect, decreasing nitrosative/oxidative stress and increasing GPx and SOD expression and activity, as well as eNOS expression. The therapeutic administration of selenium maintained this preconditioning effect up to the late phase of hypoxia-ischemia. Ccl2, Ccr2, Cxcl12, and Cxcr4 were upregulated, and long-term memory was improved. Pyknotic cells were decreased suggesting prevention of neuronal cell death. Our results show that the prophylactic zinc and therapeutic selenium administration induces effective neuroprotection in the early and late phases after CCAO.

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Clinical Significance of Serum Zinc Levels in Cerebral Ischemia

Cited by 18 publications

References 25 publications

Zinc deficiency as a possible risk factor for increased susceptibility and severe progression of Corona Virus Disease 19

Zinc deficiency as a possible risk factor for increased susceptibility and severe progression of Corona Virus Disease 19

Zinc in the central nervous system: From molecules to behavior

Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia‐Ischemia

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