Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

Ferreira, Maria Cecília de Freitas; Zucki, Fernanda; Duarte, Josilene Luciene; Iano, Flávia Godoy; Ximenes, Valdecir Farias; Buzalaf, Marília Afonso Rabelo; Oliveira, Rodrigo Cardoso de

doi:10.1002/tox.22281

Cited by 8 publications

(4 citation statements)

References 56 publications

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“…The levels of antioxidants and products can be used to measure the levels of ROS. The accumulation of ROS reduces antioxidant levels, such as those of T‐SOD and GSH, and increases MDA levels, a reaction product of ROS and lipids, in mouse bodies . In the present study, the Nrf2 pathway was activated and ROS levels increased at the early stage in the developing mice, with the increase continuing to the late stage.…”

Section: Discussionsupporting

confidence: 50%

“…The accumulation of ROS reduces antioxidant levels, such as those of T-SOD and GSH, and increases MDA levels, a reaction product of ROS and lipids, in mouse bodies. 27,28 In the present study, the Nrf2 pathway was activated and ROS levels increased at the early stage in the developing mice, with the increase continuing to the late stage. Similar changes were observed later in the adult mice than in the developing mice.…”

Section: Tio 2 Nps Induced Insulin Resistance (Ir) Earlier In Develsupporting

confidence: 52%

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The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Zhang

et al. 2019

Environmental Toxicology

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Titanium dioxide nanoparticles (TiO2 NPs) are authorized food additives, and children have the highest exposure. Therefore, children are likely more susceptible to the adverse effects of TiO2 NPs than adults. Previous study showed that oral administration of 50 mg/kg body weight (bw) TiO2 NPs increase plasma glucose in mice. However, few studies have directly compared the adverse effects of exposure to TiO2 NPs on plasma glucose metabolism of different age groups. In this study, the developing (age 3 weeks) and adult mice (age 10 weeks) were orally administered with 50 mg/kg bw TiO2 NPs per day. The TiO2 NPs induced hyperglycemia earlier in the developing mice than in the adult mice. Then mechanisms were analyzed after mice were oral administration of TiO2 NPs for 8 weeks and 26 weeks, respectively. Results showed that the treatment with TiO2 NPs activated xenobiotic biodegradation in livers of both developing and adult mice at the early stage. However, only in the developing mice, TiO2 NPs induced endoplasmic reticulum (ER) stress in livers and increased reactive oxygen species in livers and sera in the early stage. The ER stress and ROS activated an inflammation response and mitogen‐activated protein kinase pathways, thereby inducing insulin resistance in the livers of developing mice at the early stage. The response of the adult mice was delayed, and these changes were observed in the late stage of the study. The results of this study all suggest that children are more susceptible than adults to the toxicity of orally administered TiO2 NPs.

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Section: Discussionsupporting

confidence: 50%

Section: Tio 2 Nps Induced Insulin Resistance (Ir) Earlier In Develsupporting

confidence: 52%

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Zhang

et al. 2019

Environmental Toxicology

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“…4:0 ml=day=mice*0:01 mg L À1 *30 days ¼ 1:20 mg (1) 3. The changes of oxidative stress indices like MDA, SOD and GPx after low concentration toxic metal exposure individually are inconsistent with the literature in organs would not be observed if the Pb exposure concentration below 50 mg L À1 in most of studies concerning Pb exposed mice and rats (Moreira et al, 2001;Berrahal et al, 2007;Ferlemi et al, 2014;Alya et al, 2015;Ferreira et al, 2016). However, with the same chromogenic substrate assay, there is a significant change of MDA, SOD and GPx in organs after being exposed with an extremely low Pb concentration of 0.01 mg L À1 in this study (Cobbina et al, 2015b).…”

Section: The Ingestion Of Individual Toxic Metal Is Inconsistent Withmentioning

confidence: 83%

Combined exposure of low dose lead, cadmium, arsenic, and mercury in mice

2016

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“…Humans and animals are exposed to Pb in ways such as drinking water, ambient air, food, electronic waste, industrial materials, and anthropogenic activities, such as industrial sites and consumer products 11,12 . It is accepted that lead can cause health problems in different body tissues such as kidney, lung, liver, brain, and hematopoietic, nervous, and reproductive systems in animals and humans 13–21 . Lead‐induced deterioration of male reproductive health may occur 22 .…”

Section: Introductionmentioning

confidence: 99%

Effects of sinapic acid on lead acetate‐induced oxidative stress, apoptosis and inflammation in testicular tissue

Tuncer

Akarsu

Küçükler

et al. 2023

Environmental Toxicology

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In this study, the effect of lead acetate (PbAc) and sinapic acid (SNP) administration on oxidative stress, apoptosis, inflammation, sperm quality and histopathology in testicular tissue of rats was tried to be determined. PbAc was administered at a dose of 30 mg/kg/bw for 7 days to induce testicular toxicity in rats. Oral doses of 5 and 10 mg/kg/bw SNP were administered to rats for 7 days after PbAc administration. According to our findings, while PbAc administration increased MDA content in rats, it decreased GPx, SOD, CAT activity and GSH content. NF‐kB, IL‐1β, TNF‐α, and COX‐2, which are among the inflammation parameters that increased due to PbAc, decreased with the administration of SNP. Nrf2, HO‐1, and NQO1 mRNA transcript levels decreased with PbAc, but SNP treatments increased these mRNA levels in a dose‐dependent manner. RAGE and NLRP3 gene expression were upregulated in PbAc treated rats. MAPK14, MAPK15, and JNK relative mRNA levels decreased with SNP treatment in PbAc treated rats. While the levels of apoptosis markers Bax, Caspase‐3, and Apaf‐1 increased in rats treated with PbAc, the level of Bcl‐2 decreased, but SNP inhibited this apoptosis markers. PbAc caused histopathological deterioration in testis tissue and negatively affected spermatogenesis. When the sperm quality was examined, the decrease in sperm motility and spermatozoon density caused by PbAc, and the increase in the ratio of dead and abnormal spermatozoa were inhibited by SNP. As a result, while PbAc increased apoptosis and inflammation by inducing oxidative stress in testicles, SNP treatment inhibited these changes and increased sperm quality.

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Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

Cited by 8 publications

References 56 publications

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Combined exposure of low dose lead, cadmium, arsenic, and mercury in mice

Effects of sinapic acid on lead acetate‐induced oxidative stress, apoptosis and inflammation in testicular tissue

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