Plasma and Erythrocyte Magnesium, Manganese, Zinc, and Plasma Calcium Levels in G-6-PD-Deficient and Normal Male Children

Sarikcioglu, Sureyya Bilmen; Gümüşlü, Saadet; Uysal, Nimet; Aksu, Tevfik Aslan

doi:10.1385/bter:99:1-3:041

Cited by 2 publications

(3 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Required amount of MnCl 2 can be beneficial for living organisms through regulating enzymatic synthesis and promoting hematopoiesis [2,3]. It is also a fundamental ingredient for making fungicides, steel, and welding metals and many industry products [4].…”

Section: Introductionmentioning

confidence: 99%

Apoptosis Induced by Manganese on Neuronal SK-N-MC Cell Line: Endoplasmic Reticulum (ER) Stress and Mitochondria Dysfunction

Yoon

Kim

Lee

et al. 2011

Environ Health Toxicol

View full text Add to dashboard Cite

ObjectivesManganese chloride (MnCl2) is one of heavy metals for causing neurogenerative dysfunction like Manganism. The purpose of this study was to determine the acute toxicity of MnCl2 using different times and various concentrations including whether manganese toxicity may involve in two intrinsic pathways, endoplasmic reticulum (ER) stress and mitochondria dysfunction and lead to neuronal apoptosis mediated by organelle disorders in neuroblastoma cell line SK-N-MC.MethodsIn the acute toxicity test, five concentrations (200, 400, 600, 800, 1,000 uM) of MnCl2 with 3, 6, 12, 24, 48 hours exposure were selected to analyze cell viability. In addition, to better understand their toxicity, acute toxicity was examined with 1,000 uM MnCl2 for 24 hours exposure via reactive oxygen species (ROS), mitochondria membrane potential, western blotting and mitochondrial complex activities.ResultsOur results showed that both increments of dose and time prompt the increments in the number of dead cells. Cells treated by 1,000 µM MnCl2 activated 265% (±8.1) caspase-3 compared to control cell. MnCl2 induced intracellular ROS produced 168% (±2.3%) compared to that of the control cells and MnCl2 induced neurotoxicity significantly dissipated 48.9% of mitochondria membrane potential compared to the control cells.ConclusionsThis study indicated that MnCl2 induced apoptosis via ER stress and mitochondria dysfunction. In addition, MnCl2 affected only complex I except complex II, III or IV activities.

show abstract

Section: Introductionmentioning

confidence: 99%

Apoptosis Induced by Manganese on Neuronal SK-N-MC Cell Line: Endoplasmic Reticulum (ER) Stress and Mitochondria Dysfunction

Yoon

Kim

Lee

et al. 2011

Environ Health Toxicol

View full text Add to dashboard Cite

show abstract

“…Currently, there are few studies correlating blood zinc levels and G6PD deficiency. These studies (Sarikcioglu et al 2004;Honar et al 2017) reported no significant difference between G6PD normal and deficient individuals in plasma/ erythrocyte and serum/erythrocyte zinc, respectively -despite the severity of acute hemolysis. However, their study analyzed older children that are not within the age group included in this study.…”

Section: Determination Of Plasma Zinc Level Of G6pddeficient Children...mentioning

confidence: 95%

“…Zinc is also vital in the production of the antioxidant enzyme, superoxide dismutase, vitamin A, and metallothioneins (O'Dell 2000), among others -and in protecting against DNA damage (Marreiro et al 2017) and other diseases (Sarikcioglu et al 2004).…”

Section: Determination Of Plasma Zinc Level Of G6pddeficient Children...mentioning

confidence: 99%

Association of Sex and Zinc Deficiency with Glucose-6-Phosphate Dehydrogenase Deficiency in Filipino Children

Nicolas¹,

Javier²,

Litan³

et al. 2021

Philipp J Sci

View full text Add to dashboard Cite

In the Philippines, one of every 54 newborns has glucose-6-phosphate dehydrogenase (G6PD) deficiency. While most were determined to have a familial origin, at least 15% of cases have unknown etiology. This study investigated sex, regional malaria incidence, and zinc deficiency as factors contributing to the high incidence of G6PD deficiency in Filipinos. The study used both retrospective and experimental approaches. The retrospective study analyzed demographic data reported in 8,158 clean archival records from 2010–2015 of 0–5-yr-old Filipino children with G6PD deficiency; the regional distribution data from DOH of malaria was also included for possible correlation with the regional frequency of malaria in the Philippines. The experimental approach determined plasma zinc concentrations of 138 deficient and 41 normal neonates and children aged 0–11 mo using atomic absorption spectroscopy to determine if the zinc level was associated with G6PD activity. Results showed that the major peak for G6PD activity for the male cluster was at 0.5–3.5 U/g Hb, while there were two major peaks for females – one at 0.5–2.5 U/g Hb and another at 3–9.5 U/g Hb. These results are consistent with G6PD-deficiency being an X-linked disorder and for Filipinos, a sex-based reference standard in the newborn screening for G6PD activity of Filipino children is, therefore, being proposed. The incidence of malaria in the country showed no association with G6PD incidence (ρ = 0.06; p = 0.983). On the other hand, the mean plasma zinc concentration of G6PD-deficient children aged 0.5–3 mo old at 43.11 ± 1.68 μg/dL was significantly different from that of normal controls at 51.89 ± 3.00 ug/dL. These results showed, therefore, that there is a probable association between zinc deficiency and the disorder in 0–3-mo-old children, implying mother’s micronutrient health as a risk factor in the high prevalence of G6PD among Filipino children.

show abstract

Plasma and Erythrocyte Magnesium, Manganese, Zinc, and Plasma Calcium Levels in G-6-PD-Deficient and Normal Male Children

Cited by 2 publications

References 11 publications

Apoptosis Induced by Manganese on Neuronal SK-N-MC Cell Line: Endoplasmic Reticulum (ER) Stress and Mitochondria Dysfunction

Apoptosis Induced by Manganese on Neuronal SK-N-MC Cell Line: Endoplasmic Reticulum (ER) Stress and Mitochondria Dysfunction

Association of Sex and Zinc Deficiency with Glucose-6-Phosphate Dehydrogenase Deficiency in Filipino Children

Contact Info

Product

Resources

About