Tissue distribution of polaprezinc in rats determined by the double tracer method

Furuta, Shigeru; Suzuki, Masahiro; Toyama, Seiji; Miwa, Masahiro; Sano, Hiroshi

doi:10.1016/s0731-7085(98)00236-2

Cited by 5 publications

(4 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[42][43][44] Although the induction of MT by zinc has been reported in various tissues, the inability of Zn 2+ to cross the BBB limits the investigation of these effects in vivo. 45,46 These facts may explain why the level of MT in control rats injected with ZnCl 2 (i.v.) was unchanged, but increased in the brain of ischaemic rats after ZnCl 2 injection (i.v.)…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have suggested that the zinc status affects MT concentrations and mRNA synthesis in various tissues of growing and adult rats and mice 42–44 . Although the induction of MT by zinc has been reported in various tissues, the inability of Zn 2+ to cross the BBB limits the investigation of these effects in vivo 45,46 . These facts may explain why the level of MT in control rats injected with ZnCl 2 (i.v.)…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

SYSTEMIC ADMINISTRATION OF Zn²⁺ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

Helal

2008

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. The aim of the present study was to test the protective role of intravenous Zn(2+) against iron-catalysed reperfusion injury in the hippocampus of ischaemic rats. 2. One hundred adult male Wistar albino rats were randomly divided into five groups. Rats in the first group were subjected to surgery (sham operation) without induction of cerebral ischaemia and injected with normal saline (i.v.). The second group of sham-operated rats were injected with 6 mg/kg, i.v., ZnCl(2). In the third group, rats were subjected to cerebral ischaemia for 60 min. Animals in the fourth group were subjected to cerebral ischaemia for 60 min followed by 8 h reperfusion. In the fifth group, rats were subjected to cerebral ischaemia for 60 min, followed by 8 h reperfusion with injection of a single dose of ZnCl(2) (6 mg/kg, i.v.) during the first 5 min of the reperfusion period. After reperfusion, animals were killed, their brains were dissected out on ice and the two hippocampi from each animal were isolated and analysed. 3. Cerebral ischaemia induced an increase in the iron content, lipidic peroxidation, apoptosis and metallothionein (MT) in the hippocampus. These effects were significantly increased in the hippocampus of ischaemic rats subjected to 8 h reperfusion compared with ischaemic non-reperfused rats. Intravenous administration of ZnCl(2)decreased the accumulation of iron, lipidic peroxidation and apoptosis produced by reperfusion, but increased the level of MT. 4. Data from the present study suggest that, after 1 h ischaemia, there is an increase in the permeability of the blood-brain barrier and this allows penetration of i.v. injected ZnCl(2), which can induce expression of brain MT, increase the anti-oxidant capacity and diminish iron-catalysed lipid peroxidation and apoptosis. This may give new insights as to how to improve the outcome for stroke patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

SYSTEMIC ADMINISTRATION OF Zn²⁺ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

Helal

2008

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…BBB regulates zinc homeostasis in the brain. Studies have shown that under normal physiological conditions, the BBB isolates zinc between the plasma and the brain ( 235 ). Studies in animal models have shown that zinc homeostasis is critical for BBB integrity.…”

Section: Ischemic Strokementioning

confidence: 99%

Stroke-induced damage on the blood–brain barrier

Xue,

Zhou,

Yang

et al. 2023

Front. Neurol.

View full text Add to dashboard Cite

The blood–brain barrier (BBB) is a functional phenotype exhibited by the neurovascular unit (NVU). It is maintained and regulated by the interaction between cellular and non-cellular matrix components of the NVU. The BBB plays a vital role in maintaining the dynamic stability of the intracerebral microenvironment as a barrier layer at the critical interface between the blood and neural tissues. The large contact area (approximately 20 m2/1.3 kg brain) and short diffusion distance between neurons and capillaries allow endothelial cells to dominate the regulatory role. The NVU is a structural component of the BBB. Individual cells and components of the NVU work together to maintain BBB stability. One of the hallmarks of acute ischemic stroke is the disruption of the BBB, including impaired function of the tight junction and other molecules, as well as increased BBB permeability, leading to brain edema and a range of clinical symptoms. This review summarizes the cellular composition of the BBB and describes the protein composition of the barrier functional junction complex and the mechanisms regulating acute ischemic stroke-induced BBB disruption.

show abstract

“…The authors infused zinc acetate solution (1 mg Zn/ml) intravenously at a rate of 1.0 ml/min for 30 min and then continuously at 0.125 ml/min for 7 h. Data showed that the infusion increased plasma zinc (pZn) concentration approximately 10-fold without altering the zinc concentration in cerebrospinal fluid (CSF Zn), suggesting that the BBB prevented pZn from penetrating into the brain (Blair-West et al 1990). Another study in rats revealed that the replacement ratios of 65 Zn to zinc in tissues were 40% in plasma, 16-20% in liver, kidney, blood, and prostate, while the replacement ratios in testis and cerebrum were very low (2-3%), suggesting that zinc uptakes in testis and brain may be regulated by the blood-testis barrier and BBB (Furuta et al 1999).…”

Section: Plasma Zinc Across the Bbbmentioning

confidence: 99%

The interaction of zinc and the blood-brain barrier under physiological and ischemic conditions

Liu

2019

Toxicology and Applied Pharmacology

View full text Add to dashboard Cite

Zinc is the second most abundant metal in human and serves as an essential trace element in the body. During the past decades, zinc has been found to play important roles in central nervous system, such as the development of neurons and synaptic activities. An imbalance of zinc is associated with brain diseases. The blood-brain barrier (BBB) maintains the homeostasis of the microenvironment, regulating the balance of zinc in the brain. A compromised BBB is the main cause of severe complications in cerebral ischemic patients, such as hemorrhage transformation, inflammation and edema. Recent studies reported that zinc in the brain may be a potential target for integrative protection against ischemic brain injury. Although zinc has long been regarded as important transmitters in central nervous system, the critical role of zinc dyshomeostasis in damage to the BBB has not been fully recognized. In this review, we summarize the role of the BBB in regulating homeostasis of zinc in physiological conditions and the effects of changes in zinc levels on the permeability of the BBB in cerebral ischemia. The integrity of BBB maintains the homeostasis of zinc in pathological conditions, while the balance of zinc in the brain and the circulation maintains the normal function of the BBB. Interrupting the zinc/BBB system will disturb the microenvironment in the brain, leading to pathological diseases. In stroke patients, zinc may serve as a potential target for protecting the BBB and reducing hemorrhage transformation, inflammation and edema.

show abstract

Tissue distribution of polaprezinc in rats determined by the double tracer method

Cited by 5 publications

References 14 publications

SYSTEMIC ADMINISTRATION OF Zn²⁺ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

SYSTEMIC ADMINISTRATION OF Zn²⁺ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

Stroke-induced damage on the blood–brain barrier

The interaction of zinc and the blood-brain barrier under physiological and ischemic conditions

Contact Info

Product

Resources

About

Tissue distribution of polaprezinc in rats determined by the double tracer method

Cited by 5 publications

References 14 publications

SYSTEMIC ADMINISTRATION OF Zn2+ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

SYSTEMIC ADMINISTRATION OF Zn2+ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

Stroke-induced damage on the blood–brain barrier

The interaction of zinc and the blood-brain barrier under physiological and ischemic conditions

Contact Info

Product

Resources

About

SYSTEMIC ADMINISTRATION OF Zn²⁺ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY

SYSTEMIC ADMINISTRATION OF Zn²⁺ DURING THE REPERFUSION PHASE OF TRANSIENT CEREBRAL ISCHAEMIA PROTECTS RAT HIPPOCAMPUS AGAINST IRON‐CATALYSED POSTISCHAEMIC INJURY