
Zinc is an essential trace element that plays a fundamental role in human health. It is a component of several enzymes, regulates hormones and gene expression, and is a cofactor in the regulation of carbohydrate, fat and protein metabolism. It is also important for platelet aggregation and fibrin formation, and activation of the contact system.
Zinc deficiency is associated with impairment of numerous metabolic processes, reduced resistance to infections, changes in skin and its appendages, and disorders of wound healing and haemostasis.
While zinc is essential for normal brain function and repair, it has also been implicated in the neuronal damage and death that follows traumatic brain injury, stroke, and seizure.
A study on patients with ischemic stroke found that 87% of the control group had a zinc deficiency while 73.5% of stroke patients had increased zinc serum levels. Another study found that zinc deficiency was reported in 35.7% of patients with ischemic stroke.
In the animal model with transient total and forebrain ischemia, an accumulation of zinc was observed as the last step of an ischemic insult before neuronal cell death.
In recent studies in hypertensive stroke patients, a significant inverse association was found between plasma zinc and the first occurrence of haemorrhagic stroke, although this association was more pronounced in obese patients and low plasma copper.
In a retrospective analysis of 384 patients with acute subarachnoid haemorrhage, 67% were found to have reduced serum zinc levels within the first seven days after the event. The zinc deficiency was associated with a more severe course of disease.
Zinc deficiency could be a risk factor for the development of haemorrhagic strokes.
Characteristics | Values |
---|---|
Zinc deficiency | Can be a risk factor for stroke |
Zinc levels | Can be higher in stroke patients |
Zinc | Is an independent risk factor for ischemic strokes |
Zinc | Is essential for the structure and function of regulatory, structural and enzymatic proteins |
Zinc | Has neuroprotective and neurotoxic effects |
Zinc | Is a modifiable risk factor for haemorrhagic stroke |
What You'll Learn
Zinc is an important trace element in biological systems
Zinc is present in all body tissues and fluids, with approximately 60% of zinc stored in skeletal muscle, 30% in bone, and 5% in the liver and skin. It is also found in the brain, kidneys, pancreas, and heart.
Zinc is a structural constituent of about 750 zinc-finger transcription factors and is a catalytic component of all six classes of enzymes, encompassing almost 2000 enzymes in the body.
Zinc is involved in immune functions, and its deficiency results in a compromised immune system. It also plays a role in cell cycle progression, meiosis, and various physiological processes, including cell proliferation, differentiation, and apoptosis.
Zinc is also involved in the regulation of glucose metabolism, and its deficiency has been linked to diabetes and diabetic cardiomyopathy.
Zinc is an essential factor in maintaining cellular homeostasis and has been increasingly spotlighted in the context of disease development, including cancer, cardiovascular disease, autoimmune diseases, and neurodegenerative disorders.
Zinc transporters and metallothioneins play a critical role in regulating zinc homeostasis and are implicated in various diseases.
Zinc is also involved in the detoxification of heavy metals, such as cadmium and arsenic.
Zinc supplementation has been found to be beneficial in treating diarrhea, chronic hepatitis C, shigellosis, leprosy, tuberculosis, pneumonia, acute lower respiratory tract infection, common cold, and leishmaniasis.
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Zinc is a contributing factor in the pathogenesis of stroke
Zinc is an essential trace element that plays a fundamental role in human health. It is a contributing factor in the pathogenesis of stroke, with studies showing that abnormal zinc accumulation in the brain is found in various neurological diseases, including stroke.
Zinc is a component of the catalytic activity of over 300 enzymes and is an enzymatic cofactor in the regulation of carbohydrate, fat, and protein metabolism. It also plays a role in immune function, acting as a second messenger and influencing the redox metabolism.
Zinc deficiency is associated with impairment of numerous metabolic processes, reduced resistance to infections, changes in skin and its appendages, and disorders of wound healing and haemostasis. Studies have shown that zinc supplementation reduces infarct size, while zinc chelation is neurotoxic.
Zinc is released into the synaptic cleft during an ischemic stroke, leading to a sharp increase in zinc concentrations. This can trigger selective neuronal death and is a possible risk factor for the development of haemorrhagic strokes.
Zinc also has a protective effect on the vascular wall, reducing damage caused by fatty acids. It has been shown to reduce oxidative stress and cell and tissue damage, inhibit inflammatory reactions, and improve endothelial dysfunction.
In summary, zinc is a contributing factor in the pathogenesis of stroke, and its role in stroke development and treatment should be further investigated.
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Zinc is a neurotoxin
Zinc can also cause neurotoxicity by disrupting calcium homeostasis, which is crucial for neuronal survival. Zinc can induce the expression of a zinc-finger transcription factor, which in turn suppresses neural-specific target genes, including GluR2, which is involved in calcium homeostasis. Zinc can also activate signal transduction pathways, such as protein kinase C, which can promote the generation of reactive oxygen species.
Furthermore, zinc can augment glutamate-induced neuronal injury by directly inhibiting GABAA channels and inhibiting glutamate re-uptake by blocking excitatory amino acid transporters expressed on glial cells. Zinc also plays a role in endothelial dysfunction, which is a significant factor in the progression of arteriosclerosis.
However, it is important to note that zinc also has neuroprotective effects. For example, zinc supplementation can provide neuroprotection to the hippocampal subfield during global ischemia. Zinc has also been found to possess anti-inflammatory effects and can reduce ischemic brain edema.
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Zinc is a neuroprotective agent
Zinc is a trace metal ion in the central nervous system that plays important biological roles, such as in catalysis, structure, and regulation. It contributes to antioxidant function and the proper functioning of the immune system and it plays an important role in neurophysiology, which leads to cell growth and cell proliferation.
Zinc is a neuromodulator, released during synaptic transmission and it binds to presynaptic or postsynaptic membrane receptors. It is also a co-factor for many enzymes, and it affects gene expression through transcription factor regulation.
Zinc is essential for the normal development and function of cells that mediate nonspecific immunity, such as neutrophils and natural killer cells. It also has a specific activation function for Th1 cytokine production and helps B-lymphocytes.
Zinc is also essential for endothelial integrity and it has been shown to have a protective effect on damage to the vascular wall caused by fatty acids.
Zinc deficiency can lead to impairment of numerous metabolic processes, reduced resistance to infections due to impaired immune functions, changes in skin and its appendages and disorders of wound healing and haemostasis.
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Zinc is an independent risk factor for ischemic strokes
Zinc is an essential trace element that plays a fundamental role in metabolic, immunological, and other biological processes. It is also a key modulator of neuronal excitability and is involved in the regulation of numerous reactions in haemostasis and thrombosis.
Zinc has been found to be a risk factor for ischemic strokes. A study on patients with ischemic stroke found that they had lower serum zinc levels compared to a control group. Another study found that zinc deficiency may be a risk factor for ischemic stroke, especially in women. A third study found that zinc is found to be deficient in patients with ischemic stroke.
Zinc has been shown to have both neuroprotective and neurotoxic effects. Some studies have found that zinc supplementation reduces infarct size, while zinc chelation is neurotoxic.
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Frequently asked questions
Zinc is an essential trace element that plays a fundamental role in metabolic, immunological, and other biological processes. It is a key component for the catalytic activity of enzymes, a structural element for various transcription factors, and a regulator of hormones, hormone receptors, and gene expression. It also plays a role in immunity, haemostasis, and thrombosis.
Studies have shown that zinc deficiency is associated with an increased risk of stroke, particularly haemorrhagic stroke. However, the exact mechanism is still unclear, and further research is needed.
Zinc deficiency can lead to endothelial dysfunction, increased oxidative stress, and impaired wound healing, all of which are risk factors for stroke. Additionally, zinc is involved in the regulation of numerous reactions in haemostasis and thrombosis.
Clinical signs of prolonged zinc deficiency include disorders of the sense of smell and taste, dark adaptation, changes in the skin and its appendages (e.g., brittle nails, dry skin), impaired wound healing, increased susceptibility to infections, and cerebral dysfunctions.
A healthy person loses 2-3 mg of zinc daily, and the recommended daily zinc intake for adults is 7-11 mg. Zinc can be found in oysters, wheat germ, muscle meat, animal offal, potatoes, and wholemeal bread. However, the bioavailability of zinc in certain foods may be limited. To prevent or treat zinc deficiency, a controlled zinc supplement may be recommended.