Gallium and Gallium Semiconductor Compounds

Fowler, Bruce A.; Sexton, Mary

doi:10.1016/b978-0-444-59453-2.00036-6

Cited by 4 publications

(1 citation statement)

References 144 publications

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“…It has been estimated that around 140 million people are exposed to arsenic, a metalloid world over by contaminated water (Kris, 2009). Besides, arsenic has anthropogenic uses as an alloying agent in the manufacture of electronic transistors and semiconductors, wood preservatives, metal adhesives and pigments (Fowler and Sexton, 2007; Wlodarczyk et al, 2011). Mining, smelting of ores, burning of fossil fuels, weathering and volcanic eruptions also significantly contribute to introduce arsenic in the environment (Vall et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Early life arsenic exposure and brain dopaminergic alterations in rats

Chandravanshi

Shukla

Sultana

et al. 2014

Intl J of Devlp Neuroscience

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Recently, we found that early life exposure to arsenic at low doses resulted to cause brain cholinergic deficits and exhibited a trend of recovery on withdrawal of arsenic exposure. In continuation to this, the present study has been carried out to assess the impact of low level arsenic exposure on brain dopaminergic system and associated behavior in developing rats and investigate if neurobehavioral changes are recovered or persistent. Early life exposure (PD22-PD59) to arsenic (2 or 4 mg/kg body weight, p.o.) in rats resulted to increase the motor activity on PD60, compared to controls. The hyperactivity in arsenic exposed rats was found to be linked with increase in the binding of DA-D2 receptors (38%, 56%), mRNA expression of DAR-D2 receptor gene (68%, 97%) and expression of tyrosine hydroxylase protein (1.93, 2.73-fold) in the corpus striatum as compared to controls on PD60. Exposure to arsenic enhanced generation of ROS (47%, 84%) and was associated with decrease in the mitochondrial membrane potential (13.3%, 15.33%), activity of mitochondrial complexes and increased oxidative stress. Disruption in the expression of pro-apoptotic, anti-apoptotic and stress marker proteins was also distinct in the corpus striatum of arsenic exposed rats. The severity of changes in the behavioral and neurochemical endpoints were found to persist in rats exposed to arsenic at high dose and exhibited a trend of recovery at low dose on withdrawal of arsenic exposure on PD90. Early life arsenic exposure appears to be critical and vulnerable as development of dopamine receptors continues during this period.

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Section: Introductionmentioning

confidence: 99%

Early life arsenic exposure and brain dopaminergic alterations in rats

Chandravanshi

Shukla

Sultana

et al. 2014

Intl J of Devlp Neuroscience

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Arsenic, Antimony, and Bismuth

Madden

Fowler²

2023

Patty's Toxicology

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Arsenic, Antimony, and Bismuth are members of Group V of the Periodic Table of Elements. These elements have been used for a variety of medicinal and pest control purposes over a number of centuries. They have also been used in metallic alloys and in the production of III–V semiconductors to increase electronic speeds of computer chips. Arsenicals are largely metabolized by methylation pathways and bismuth is known to induce the metal‐binding protein metallothionein and to form electron–dense cytoplasmic and intranuclear inclusion bodies.

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Chelation Therapy in the Treatment of Metal Intoxication

Aaseth¹,

Crisponi

Andersen³

2016

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Gallium and Gallium Semiconductor Compounds

Cited by 4 publications

References 144 publications

Early life arsenic exposure and brain dopaminergic alterations in rats

Early life arsenic exposure and brain dopaminergic alterations in rats

Arsenic, Antimony, and Bismuth

Chelation Therapy in the Treatment of Metal Intoxication

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