Arsenite-induced formation of hydroxyl radical in the striatum of awake rats

García-Chávez, Erika; Santamarı́a, Abel; Dı́az-Barriga, Fernando; Mandeville, Peter B; Juárez, Bertha I.; Jiménez‐Capdeville, María E.

doi:10.1016/s0006-8993(03)02697-0

Cited by 62 publications

(33 citation statements)

References 58 publications

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“…The enhancement of reactive oxygen species (ROS) and lipid peroxidation and the decreases in the activity of superoxide dismutase and glutathione-related enzymes induced by As could change the cellular redox status and lead to impairments of neurobehavioral function [35][36][37][38][39]. Arsenic is as a known neurotoxicant and is able to transverse the placental barrier and reaches to the conceptus in the case of maternal exposure and also crossed the blood-brain barrier (BBB) easily in our previous studies [40,41] and other researches [39,[42][43].…”

Section: Introductionmentioning

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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To better understand the effect of arsenic on central nervous system by prenatal and early life exposure, the oxidative stress and neurotransmitter metabolic enzymes were determined in offspring rats' brain cortex and hippocampus. Forty-eight pregnant rats were randomly divided into four groups, each group was given free access to drinking water that contained 0, 10, 50, and 100 mg/L NaAsO(2) from gestation day 6 (GD 6) until postnatal day 42 (PND 42). Once pups were weaned, they started to drink the same arsenic (As)-containing water as the dams. The level of malondialdehyde in 100 mg/L As-exposed pup's brain on PND 0 and cortex on PND 28 and 42 were significantly higher than in the control group (p < 0.05). Reduced glutathione (GSH) levels showed a clear decreasing trend in pup's cortex and hippocampus on PND 42. Activity of acetylcholinesterase was significantly higher in 100 mg/L As-exposed pup's hippocampus than in control group on PND 28 and 42. mRNA expression of glutamate decarboxylase (GAD(65) and GAD(67)) in 100 mg/L As-exposed pup's cortex or hippocampus on PND 28 and 42 were significantly higher than in control (p < 0.05). These alterations in the neurotransmitters and reduced antioxidant defence may lead to neurobehavioral and learning and memory changes in offspring rats.

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Section: Introductionmentioning

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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“…Arsenite is an environmental toxin that causes multiple developmental and postnatal defects in the CNS (16,23,31,83,89). When it was fed to rats, numerous areas of the brain showed increased evidence of reactive oxygen species production, in keeping with its known pro-oxidant activity (86).…”

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confidence: 99%

Mutually Exclusive Subsets of BH3-Only Proteins Are Activated by the p53 and c-Jun N-Terminal Kinase/c-Jun Signaling Pathways during Cortical Neuron Apoptosis Induced by Arsenite

Wong

Fricker

Wyttenbach

et al. 2005

Molecular and Cellular Biology

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The c-Jun N-terminal protein kinase (JNK)/c-Jun and p53 pathways form distinct death-signaling modules in neurons that culminate in Bax-dependent apoptosis. To investigate whether this signaling autonomy is due to recruitment of particular BH3-only proteins, we searched for a toxic signal that would activate both pathways in the same set of neurons. We show that arsenite activates both the JNK/c-Jun and p53 pathways in cortical neurons, which together account for >95% of apoptosis, as determined by using the mixed-lineage kinase (JNK/c-Jun) pathway inhibitor CEP11004 and p53-null mice. Despite the coexistence of both pathways in at least 30% of the population, Bim mRNA and protein expression was increased only by the JNK/c-Jun signaling pathway, whereas Noxa and Puma mRNA and Puma protein expression was entirely JNK/c-Jun independent. About 50% of Puma/Noxa expression was p53 dependent, with the remaining signal being independent of both pathways and possibly facilitated by arsenite-induced reduction in P-Akt. However, functionally, Puma was predominant in mediating Bax-dependent apoptosis, as evidenced by the fact that more than 90% of apoptosis was prevented in Puma-null neurons, although Bim was still upregulated, while Bimand Noxa-null neurons died similarly to wild-type neurons. Thus, the p53 and JNK/c-Jun pathways can activate mutually exclusive subclasses of BH3-only proteins in the same set of neurons. However, other factors besides expression may determine which BH3-only proteins mediate apoptosis.

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“…A notable decrease was detected in the activities of the enzymes and in the levels of other metabolites together with a significant increase in the lipid peroxidation, glycogen and inorganic arsenic levels after arsenic administration. Supplementation of vitamin A to the arsenic treated mice brought about no significant variation in these antioxidant and metabolic indices in comparison to that of control, revealing amelioration by vitamin A on arsenic exerted metabolic and neurotoxic effects in mice.Key words ---arsenic, vitamin A, antioxidant system, metabolic and neurotoxic effect in part by inducing rapid burst of reactive oxygen species (ROS) in mammalian cells, resulting in oxidative stress 12,13) and carcinogenesis in man. 14) Studies document that arsenic generates ROS such as hydrogen peroxide, superoxide (O 2…”

mentioning

confidence: 99%

“…Key words ---arsenic, vitamin A, antioxidant system, metabolic and neurotoxic effect in part by inducing rapid burst of reactive oxygen species (ROS) in mammalian cells, resulting in oxidative stress 12,13) and carcinogenesis in man. 14) Studies document that arsenic generates ROS such as hydrogen peroxide, superoxide (O 2…”

mentioning

confidence: 99%

Amelioration by Vitamin A upon Arsenic Induced Metabolic and Neurotoxic Effects

Gopalkrishnan

Rao

2006

JOURNAL OF HEALTH SCIENCE

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Arsenic effect was studied at two dosage levels (0.5 mg and 1 mg/kg) for 45 days in two regions of brain, viz., cerebral hemisphere (CH) and cerebellum (C) in adult mice. This study included the antioxidant profile namely superoxide dismutase (SOD), catalase, lipid peroxidation, reduced glutathione, ascorbic acid and total sulphydryl groups. Adenosine triphosphatase (ATPase), succinic dehydrogenase (SDH), phosphorylase together with glycogen and protein levels were also estimated as metabolic indices in the brain regions of mice. A notable decrease was detected in the activities of the enzymes and in the levels of other metabolites together with a significant increase in the lipid peroxidation, glycogen and inorganic arsenic levels after arsenic administration. Supplementation of vitamin A to the arsenic treated mice brought about no significant variation in these antioxidant and metabolic indices in comparison to that of control, revealing amelioration by vitamin A on arsenic exerted metabolic and neurotoxic effects in mice.Key words ---arsenic, vitamin A, antioxidant system, metabolic and neurotoxic effect in part by inducing rapid burst of reactive oxygen species (ROS) in mammalian cells, resulting in oxidative stress 12,13) and carcinogenesis in man. 14) Studies document that arsenic generates ROS such as hydrogen peroxide, superoxide (O 2•-), hydroxyl (OH • ) and peroxyl (ROO • ) radicals. 13) These free radicals and the other reactive species are constantly produced in the brain in vivo.15) Experiments on human fetal brain explants on exposure to arsenic in culture have showed disturbances in lipid peroxidation, generation of ROS and apoptosis. 16) Adenosine triphosphatase (ATPase) and succinic dehydrogenase (SDH) (enzymes of the inner mitochondrial membrane) are concerned with respiration, and energy generation; hence, are essential for cell survival. Respiratory chain is the major source of ROS, hence mitochondrial oxidative damage is thought to be a proximal cause of metabolic effects. 17,18) Metabolism in fish brain was also affected by arsenic poisoning 19) in addition to other pathological effects in general metabolism of animal tissues. 20)

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Arsenite-induced formation of hydroxyl radical in the striatum of awake rats

Cited by 62 publications

References 58 publications

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Mutually Exclusive Subsets of BH3-Only Proteins Are Activated by the p53 and c-Jun N-Terminal Kinase/c-Jun Signaling Pathways during Cortical Neuron Apoptosis Induced by Arsenite

Amelioration by Vitamin A upon Arsenic Induced Metabolic and Neurotoxic Effects

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