Chromium(VI) induces oxidative stress in the mouse brain

Travacio, Marina; Polo, José M.; Llesuy, Susana

doi:10.1016/s0300-483x(00)00254-7

Cited by 81 publications

(38 citation statements)

References 29 publications

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“…Normally the brain has moderately poor antioxidant defense (Mates, 2000) and it contains large amounts of polyunsaturated fatty acids and consumes 20% of the body's oxygen (Travacio et al, 2000). In the present study, arsenic intoxication induced a high degree of ROS production, lipid peroxidation and also protein damage like increased PC content in the various region of brain tissue of the experimental rats due to the susceptibility of the brain tissue toward oxidative damage.…”

Section: Discussionsupporting

confidence: 47%

Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

Muthu

Chanu

Shagirtha³

et al. 2016

IJPT

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Arsenic (As) is an environmental toxic metalloid that is present in everywhere such as air, water and soil. Generally, inorganic arsenic has a tendency to be more toxic than organic arsenic. The present study was designed to determine whether oral administration of silibinin (SB), which has been shown to have substantial antioxidant properties, when pre-administered (75 mg/kg body weight) once daily for 4 weeks along with arsenic (5 mg/kg) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-S-transferase (GST),glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione (GSH), total sulfhydryl groups (TSH) and vitamin C in rat brain regions such as cortex, striatum, cerebellum, hippocampus and brain stem. Our study also examined the effect of SB over arsenic-induced reactive oxygen species (ROS) production and lipid peroxidation level (LPO) and protein carbonyl content (PC) in distinct brain regions of rats. Moreover, As also alters the lipid profiles such as total lipids, phospholipids, cholesterol, cerebrosides and gangliosides in various regions of the brain. Pre-administration of SB restores the altered enzymatic and non-enzymatic antioxidants, lipid profiles and also markedly reduced the ROS, LPO, PC and accumulation of As in various regions of the brain. These results suggested that arsenic-induced deficits in antioxidant enzyme activities and increase in ROS production and lipid peroxidation levels in brain regions can be remarkably prevented by pre-administration of SB.

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Section: Discussionsupporting

confidence: 47%

Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

Muthu

Chanu

Shagirtha³

et al. 2016

IJPT

View full text Add to dashboard Cite

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“…In particular, the effect may reduce the levels of non-enzymatic antioxidants, while antioxidant enzyme activities increase as an adaptive brain response against the oxidative stress (9). Here the use of a very high dose in one animal led to clonic convulsions within 24 hr.…”

Section: Discussionmentioning

confidence: 96%

Chromium(VI) as a novel MRI contrast agent for cerebral white matter: Preliminary results in mouse brain in vivo

Watanabe

Tammer

Boretius

et al. 2006

Magnetic Resonance in Med

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This work demonstrates that intraventricular microinjections of a low dose of potassium dichromate (0.4 L of 10 mM solution) yield a specific contrast enhancement of white matter (WM) tracts in T 1 -weighted 3D MRI of mouse brain in vivo. Pronounced and persistent signal increases (40 -100% at 24 hr after injection) were observed in the corpus callosum, anterior commissure, fornix, and stria medullaris, as well as in the mammillothalamic tract and fasciculus retroflexus. These results suggest that the extracellular diffusion of diamagnetic chromium(VI) (Cr(VI)) after injection is followed by a tissue-specific reduction to paramagnetic Cr(V) and ( In neuroanatomy, specific chemical reactions of lipids exposed to aqueous solutions of potassium dichromate (K 2 Cr 2 O 7 with chromium in redox state Cr(VI)) have been used for histological staining of myelin. For example, in a previous study based on Weigert-Smith-Dietrich procedures, myelin sheaths in white matter (WM) tracts in rat brain were identified by controlled chromation of lipids, which was accompanied by a simultaneous reduction of Cr(VI) (1). The present work attempts to exploit such principles for cerebral MRI of WM. The idea is based on the assumption that a reduction of diamagnetic Cr(VI) to paramagnetic Cr(V) and Cr(III) by lipid oxidation causes a shortening of the T 1 relaxation time of surrounding water and/or lipid protons.Using sodium dichromate to study the metabolism of chromium species in biochemical reactions occurring on the skin of living rats, Liu and coworkers (2) demonstrated the potential of Cr(VI) for in vivo EPR spectroscopy. Similarly, the formation of Cr(V) and Cr(III) was detected by MRI after injection of sodium dichromate in the kidney and liver of a mouse in vivo (3), and of potassium chromate in the lung of a rat postmortem (4). The purposes of this first Cr(VI)-enhanced MRI study of mouse brain in vivo were to 1) examine whether a direct injection of a small amount of Cr(VI) induces a contrast enhancement detectable by T 1 -weighted 3D MRI, 2) determine the structures highlighted in the intact living brain, and 3) discuss putative histochemical and physiological mechanisms and how they differ from other paramagnetic MRI contrast agents.

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“…Oxidative stress in mouse brain was induced as previously described (Travacio et al, 2000). In short, 25 mg/kg per day potassium dichromate (Chromium(VI); Merck) was applied in drinking water for 3 days.…”

Section: Chromium Treatmentmentioning

confidence: 99%

Mitochondrial impairments contribute to Spinocerebellar ataxia type 1 progression and can be ameliorated by the mitochondria-targeted antioxidant MitoQ

Stucki

Ruegsegger

Steiner

et al. 2016

Free Radical Biology and Medicine

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Mitochondrial impairments contribute to Spinocerebellar ataxia type 1 progression and can be ameliorated by the mitochondria-targeted antioxidant MitoQ, Free Radical Biology and Medicine, http://dx.doi.org/10.1016/j.freeradbiomed.2016.07.005 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Chromium(VI) induces oxidative stress in the mouse brain

Cited by 81 publications

References 29 publications

Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

Chromium(VI) as a novel MRI contrast agent for cerebral white matter: Preliminary results in mouse brain in vivo

Mitochondrial impairments contribute to Spinocerebellar ataxia type 1 progression and can be ameliorated by the mitochondria-targeted antioxidant MitoQ

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