Age-Related Alterations in Antioxidant Enzymes, Lipid Peroxide Levels, and Somatosensory-Evoked Potentials: Effect of Sulfur Dioxide

Yargiçoğlu, Pi̇raye; Ağar, Ayşel; Gümüşlü, Saadet; Bîlmen, Süreyya; Oğuz, Yurttaş

doi:10.1007/s002449900552

Cited by 38 publications

(3 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other studies have reported that prenatal SO 2 exposure is associated with poor or impaired neurodevelopment in early childhood [ 44 , 45 ]. It is known that SO 2 may lead to neurotoxicity by inducing oxidative stress, DNA damage, and apoptosis, as well as DNA methylation [ 46 , 47 , 48 , 49 , 50 ]. Previous studies on the absorption, distribution, and retention of SO 2 in mammalian subjects have indicated that sulfur can be absorbed into the blood circulation and transported to the central nervous system [ 51 , 52 ].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Maternal Exposure to Air Pollutants and Heavy Metals during Pregnancy on the Risk of Neurological Disorders Using the National Health Insurance Claims Data of South Korea

et al. 2023

View full text Add to dashboard Cite

The objective of this study was to evaluate the effects of high levels of maternal exposure to ambient air pollution and heavy metals on risks of autism spectrum disorder (ASD) and epilepsy using the National Health Insurance claims data of South Korea. The data of mothers and their newborns from 2016 to 2018 provided by the National Health Insurance Service were used (n = 843,134). Data on exposure to ambient air pollutants (PM2.5, CO, SO2, NO2, and O3) and heavy metals (Pb, Cd, Cr, Cu, Mn, Fe, Ni, and As) during pregnancy were matched based on the mother’s National Health Insurance registration area. SO2 (OR: 2.723, 95% CI: 1.971–3.761) and Pb (OR: 1.063, 95% CI: 1.019–1.11) were more closely associated with the incidence of ASD when infants were exposed to them in the third trimester of pregnancy. Pb (OR: 1.109, 95% CI: 1.043–1.179) in the first trimester of pregnancy and Cd (OR: 2.193, 95% CI: 1.074–4.477) in the third trimester of pregnancy were associated with the incidence of epilepsy. Thus, exposure to SO2, NO2, and Pb during pregnancy could affect the development of a neurologic disorder based on the timing of exposure, suggesting a relationship with fetal development. However, further research is needed.

show abstract

Section: Discussionmentioning

confidence: 99%

The Effect of Maternal Exposure to Air Pollutants and Heavy Metals during Pregnancy on the Risk of Neurological Disorders Using the National Health Insurance Claims Data of South Korea

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Yargicoğlu et al. (1999) reported that sulfur dioxide inhalation exposure, to an exposure calculated to correspond to an internal dose of 1.2 mg/kg bw per day, increased brain oxidative stress (increased lipid peroxidation and Cu/Zn superoxide dismutase (SOD), decreased GSH‐Px activity) in young, middle‐aged and old rats, and impaired nerve conduction velocity (prolonged SEP latency) in young animals only. The lack of effect of sulfur dioxide on SEPs in older animals is possibly a ‘floor’ 18 effect, since latencies were also significantly prolonged in older controls compared to young controls.…”

Section: Assessmentmentioning

confidence: 99%

Follow‐up of the re‐evaluation of sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228)

Younes¹,

Aquilina²,

Castle³

et al. 2022

EFS2

View full text Add to dashboard Cite

Sulfur dioxide–sulfites (E 220–228) were re‐evaluated in 2016, resulting in the setting of a temporary ADI of 0.7 mg SO2 equivalents/kg bw per day. Following a European Commission call for data, the present follow‐up opinion assesses data provided by interested business operators (IBOs) and additional evidence identified in the publicly available literature. No new biological or toxicological data addressing the data gaps described in the re‐evaluation were submitted by IBOs. Taking into account data identified from the literature search, the Panel concluded that there was no substantial reduction in the uncertainties previously identified in the re‐evaluation. Therefore, the Panel considered that the available toxicity database was inadequate to derive an ADI and withdrew the current temporary group acceptable daily intake (ADI). A margin of exposure (MOE) approach was considered appropriate to assess the risk for these food additives. A lower confidence limit of the benchmark dose of 38 mg SO2 equivalents/kg bw per day, which is lower than the previous reference point of 70 mg SO2 equivalents/kg bw per day, was estimated based on prolonged visual evoked potential latency. An assessment factor of 80 was applied for the assessment of the MoE. At the estimated dietary exposures, when using a refined exposure scenario (Data set D), MOEs at the maximum of 95th percentile ranges were below 80 for all population groups except for adolescents. The dietary exposures estimated using the maximum permitted levels would result in MOEs below 80 in all population groups at the maximum of the ranges of the mean, and for most of the population groups at both minimum and maximum of the ranges at the 95th percentile. The Panel concluded that this raises a safety concern for both dietary exposure scenarios. The Panel also performed a risk assessment for toxic elements present in sulfur dioxide–sulfites (E 220–228), based on data submitted by IBOs, and concluded that the maximum limits in the EU specifications for arsenic, lead and mercury should be lowered and a maximum limit for cadmium should be introduced.

show abstract

“…When inhaled, SO 2 can be hydrated to sulfurous acid that then dissociates to produce sulfite/bisulfite and hydrogen ions; bisulfite can produce sulfur trioxide radical anions that react with oxygen leading to peroxyl radicals. When administered as SO 2 to young (3 mos), middle-aged (12 mos) or old (24 mos) Swiss albino rats (sex not specified) at 10 ppm for 1 h/day for 7 days/week for 6 weeks, increases in the antioxidant enzyme Cu, Zn-SOD and decreases in glutathione peroxidase were seen in all three age groups, as were increases in the lipid peroxidation marker, thiobarbituric acid reactive substances (TBARS) [463,464]. In contrast, reductions in these measures were seen in a study that exposed Kunming albino mice of both sexes to 22, 56 or 112 mg/m 3 of SO 2 for 6 h day for 7 days, with no systematic evidence of sex differences [465][466][467].…”

Section: Current Evidence That Ap-related Metals and Trace Elements C...mentioning

confidence: 99%

Air Pollution-Related Brain Metal Dyshomeostasis as a Potential Risk Factor for Neurodevelopmental Disorders and Neurodegenerative Diseases

2020

View full text Add to dashboard Cite

Increasing evidence links air pollution (AP) exposure to effects on the central nervous system structure and function. Particulate matter AP, especially the ultrafine (nanoparticle) components, can carry numerous metal and trace element contaminants that can reach the brain in utero and after birth. Excess brain exposure to either essential or non-essential elements can result in brain dyshomeostasis, which has been implicated in both neurodevelopmental disorders (NDDs; autism spectrum disorder, schizophrenia, and attention deficit hyperactivity disorder) and neurodegenerative diseases (NDGDs; Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis). This review summarizes the current understanding of the extent to which the inhalational or intranasal instillation of metals reproduces in vivo the shared features of NDDs and NDGDs, including enlarged lateral ventricles, alterations in myelination, glutamatergic dysfunction, neuronal cell death, inflammation, microglial activation, oxidative stress, mitochondrial dysfunction, altered social behaviors, cognitive dysfunction, and impulsivity. Although evidence is limited to date, neuronal cell death, oxidative stress, and mitochondrial dysfunction are reproduced by numerous metals. Understanding the specific contribution of metals/trace elements to this neurotoxicity can guide the development of more realistic animal exposure models of human AP exposure and consequently lead to a more meaningful approach to mechanistic studies, potential intervention strategies, and regulatory requirements.

show abstract

Age-Related Alterations in Antioxidant Enzymes, Lipid Peroxide Levels, and Somatosensory-Evoked Potentials: Effect of Sulfur Dioxide

Cited by 38 publications

References 42 publications

The Effect of Maternal Exposure to Air Pollutants and Heavy Metals during Pregnancy on the Risk of Neurological Disorders Using the National Health Insurance Claims Data of South Korea

The Effect of Maternal Exposure to Air Pollutants and Heavy Metals during Pregnancy on the Risk of Neurological Disorders Using the National Health Insurance Claims Data of South Korea

Follow‐up of the re‐evaluation of sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228)

Air Pollution-Related Brain Metal Dyshomeostasis as a Potential Risk Factor for Neurodevelopmental Disorders and Neurodegenerative Diseases

Contact Info

Product

Resources

About