Pharmaceutical and Biomedical Research

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Showing 3 results for Zinc

Serum zinc and copper levels in children with febrile convulsion

Mohammad Shokrzadeh, Ali Abbaskhaniyan, Mohammadreza Rafati, Mahdi Mashhadiakabr, Ali Arab,
Volume 2, Issue 3 (9-2016)

Abstract

Febrile convulsions (FC) are the most common neurologic disorder in children 6-60 months of age. Zinc (Zn) and copper (Cu) play role as cofactors in more than 300 enzymatic activities significantly. The aim of this study was to evaluate the relationship serum levels of Zn and Cu with seizure occurrence in febrile children. In this case-control study, 270 children with 6 month to 6 years were evaluated. The patients were enrolled in three groups: a) children with febrile convulsion, b) febrile children without convulsion and c) healthy ones. After recording of all patients’ characteristics, 5 mL blood was taken from peripheral vessels at the first 12 hours of hospitalization. Absorption of all samples was read by BRAIC (Rayleigh instrument) company, WFX-130 model with calibration diagram, considering samples dilution levels. The mean of serum Zn levels in children with FC were significantly lower than other two groups. Mean serum Cu levels in children with FC and non-FC patients were significantly higher than healthy children. No meaningful differences were observed in serum levels of Zn and Cu among the girl or boy cases. This study showed significant lower serum zinc level in children with febrile seizure and meaningful higher serum copper level than control group cases. There was no significant difference in level of serum zinc and copper in term of sex.

The Exposure and Hazards of Zinc Oxide Nanoparticles: In Vitro and In Vivo Studies

Parisa Saberi-Hasanabadi, Obeid M Malekshah, Hamidreza Mohammadi,
Volume 9, Issue 2 (3-2023)

Abstract

Background: Extensive application of zinc oxide nanoparticles has increased the likelihood of its release into the environment and subsequent human exposure and toxicity. The toxicity is thought to be a combined effect of intracellular particles and the release of dissolved zinc ions.
Objectives: This review outlines the possible mechanisms of zinc oxide toxicity in biological organs through in vitro and in vivo experiments.
Methods: We reviewed articles published between 2001 and 2021. In this way, we did a manual search of Google Scholar and scientific databases, including PubMed, Web of Science, Scopus, and Embase, with keywords such as “zinc oxide nanoparticles”, “toxicity mechanism”, and “in vivo and in vitro studies”. The other qualified papers contained the history of identifying zinc oxide nanoparticles, the toxicity of metallic nanoparticles, and physical, chemical, and biological side effects with topical and systematic approaches.
Results: The main mechanism suggested for zinc-based nanoparticles-induced cell damage is via the induction of increased levels of reactive oxygen species, which are oxidative stress markers. This mechanism has also been found to be a key mechanism for the cytotoxicity of other metal nanomaterials. Zinc-based nanoparticles were found to induce oxidative DNA damage, inflammation, progressive degenerative cell changes, cell cycle arrest, cytogenetic alterations, and ROS-triggered mitochondria-mediated apoptosis in human organs.
Conclusion: This review sheds light on the full understanding of in vitro and in vivo toxicity assessment of zinc oxide nanoparticles, highlighting the health concerns from the perspective of ZnO nanoparticles release to the ecosystem after their increasing application.

Interaction of Dorsal Hippocampal Nicotinic Receptors and Zinc Oxide Nanoparticles on Memory Consolidation

Niloufar Darbandi, Ahmad Sadeghi, Farzaneh Nazari-Serenjeh, Zahra Ghasemzadeh,
Volume 10, Issue 4 (10-2024)

Abstract

Background: Zinc oxide nanoparticles (ZnO NPs) are widely used in industry, medicine, and agriculture. Previous studies have shown that exposure to ZnO NPs can induce changes in learning and memory. Nicotinic receptors in the dorsal hippocampus are involved in drug-induced effects on memory formation.
Objectives: The present study investigates the possible role of dorsal hippocampal nicotinic receptors in the effects of ZnO NPs on memory consolidation.
Methods: Animals were bilaterally cannulated in the CA1 regions of the hippocampus. Saline, nicotine, and mecamylamine (a non-selective antagonist of nicotinic acetylcholine receptors) were administered immediately after training (intracerebral), and intraperitoneal injections of saline or ZnO NPs were given at 5-min intervals. Memory and motor activity were assessed using the passive avoidance test and the open field test, respectively.
Results: Post-training intra-CA1 microinjection of nicotine improved the amnesia induced by ZnO NPs. Mecamylamine potentiated the effects of an ineffective dose of ZnO NPs on memory consolidation.
Conclusion: ZnO NPs impair memory through interactions with nicotinic receptors in the dorsal hippocampus.

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