Prenatal cocaine administration increases glutathione and alpha-tocopherol oxidation in fetal rat brain

Lipton, Jack W.; Gyawali, Sandeep; Borys, Ewa; Koprich, James B.; Ptaszny, Magdalena E.; McGuire, Susan O.

doi:10.1016/j.devbrainres.2003.08.006

Cited by 42 publications

(22 citation statements)

References 47 publications

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“…The GSH/GSSG ratios of ϳ200 found in brains exposed to 37°C or 4°C for 2 min are within the range of values reported previously in brains from normal young rats (Lipton et al, 2003;Calabrese et al, 2004). The maintenance of GHS/GSSG ratios of ϳ200 for at least 5 min at 4°C strongly suggests that brain incubation at low temperature prevents the change in global cellular redox state produced by our model of cerebral ischemia, probably by reducing free radical formation (Lei et al, 1997;McManus et al, 2004).…”

Section: Brain Tissue Redox State During Ischemiasupporting

confidence: 64%

Ischemia Enhances Activation by Ca²⁺and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Bull¹,

Finkelstein²,

Gálvez³

et al. 2008

J. Neurosci.

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Cerebral ischemia stimulates] changes. Endoplasmic reticulum vesicles were isolated from the cortex of rat brains incubated without blood flow for 5 min at 37°C (ischemic) or at 4°C (control). Ischemic brains displayed increased oxidative intracellular conditions, as evidenced by a lower ratio (ϳ130:1) of reduced/oxidized glutathione than controls (ϳ200:1). Single RyR channels from ischemic or control brains displayed the same three responses to Ca 2ϩ reported previously, characterized by low, moderate, or high maximal activity. Relative to controls, RyR channels from ischemic brains displayed with increased frequency the high activity response and with lower frequency the low activity response. Both control and ischemic cortical vesicles contained the RyR2 and RyR3 isoforms in a 3:1 proportion, with undetectable amounts of RyR1. Ischemia reduced [ 3 H]ryanodine binding and total RyR protein content by 35%, and increased at least twofold endogenous RyR2 S-nitrosylation and S-glutathionylation without affecting the corresponding RyR3 endogenous levels. In vitro RyR S-glutathionylation but not S-nitrosylation favored the emergence of high activity channels. We propose that ischemia, by enhancing RyR2 S-glutathionylation, allows RyR2 to sustain CICR; the resulting amplification of Ca 2ϩ entry signals may contribute to cortical neuronal death.

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Section: Brain Tissue Redox State During Ischemiasupporting

confidence: 64%

Ischemia Enhances Activation by Ca²⁺and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Bull¹,

Finkelstein²,

Gálvez³

et al. 2008

J. Neurosci.

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“…The ratios in this study (31 to 57) are clearly within this range. Among the factors that may contribute to this range are strain of rat, age, tissue preparation, and the methodology that was employed to assess GSH and GSSG (Lin et al, 2002;Lipton et al, 2003;Samuele et al, 2005). In the present study, the reduction in GSH/GSSG ratio in aged rats suggested a deficiency in the aged brains to detoxify the ROS, which normally occurs in the brain (Dringen et al, 2000), or resulting from neurotoxin insults.…”

Section: Age Effects On Gsh Gssg and Gsh/gssg Ratio In Rat Brainmentioning

confidence: 60%

“…The decrease in GSH level and increase in GSSG level in aged rats produces a significant decrease in the GSH/GSSG ratio, which is often used to indicate the redox state within the tissue (Dringen et al, 2000;Lin et al, 2002;Samuele et al, 2005). In previous studies, the ratios of GSH/GSSG spread from 7 to 200 (Lin et al, 2002;Lipton et al, 2003;Samuele et al, 2005). The ratios in this study (31 to 57) are clearly within this range.…”

Section: Age Effects On Gsh Gssg and Gsh/gssg Ratio In Rat Brainmentioning

confidence: 78%

Age-related changes in glutathione and glutathione-related enzymes in rat brain

2006

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The most reliable and robust risk factor for some neurodegenerative diseases is aging. It has been proposed that processes of aging are associated with the generation of reactive oxygen species and a disturbance of glutathione homeostasis in the brain. Yet, aged animals have rarely been used to model the diseases that are considered to be age-related such as Parkinson's or Alzheimer's disease. This suggests that the results from these studies would be more valuable if aged animals were used. The present study was designed to provide insight into the glutathione redox state in young and aged rat siblings of both genders by studying the enzyme activities related to glutathione synthesis, cycling, and usage. The results suggested a significant age-related reduction of reduced glutathione (GSH) level in all brain regions examined, associated with an increase of GSH oxidation to glutathione disulfide (GSSG) and decrease of the GSH/GSSG ratio. These changes were accompanied by diminished γ-glutamylcysteine synthetase activity in de novo glutathione synthesis and increased lipid peroxidation. In addition, these changes were associated with increased enzyme activities related to the GSH usage (glutathione peroxidase, γ-glutamyl transpeptidase, and glutathione Stransferase). The results indicate that aged animals are likely more vulnerable to oxidative stress and insinuate the roles of aged animals in modeling age-related neurodegeneration diseases.

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“…Cocaine exposure also induced a lower catalase activity in the PFC and striatum in mice (Macedo et al, 2005), but higher superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in the same brain areas in rats (Dietrich et al, 2005). Nonenzymatic antioxidant levels such as reduced glutathione (GSH) or vitamin (vit) E, were also decreased upon cocaine exposure (Lipton et al, 2003;Poon et al, 2007). GSH concentration and GPx activity were decreased in the hippocampus of cocainetreated animals (Muriach et al, 2010).…”

Section: Cocaine and Oxidative Stressmentioning

confidence: 89%

Role of Mitochondria on the Neurological Effects of Cocaine

Pereira

Cunha‐Oliveira

2017

The Neuroscience of Cocaine

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Prenatal cocaine administration increases glutathione and alpha-tocopherol oxidation in fetal rat brain

Cited by 42 publications

References 47 publications

Ischemia Enhances Activation by Ca²⁺and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Ischemia Enhances Activation by Ca²⁺and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Age-related changes in glutathione and glutathione-related enzymes in rat brain

Role of Mitochondria on the Neurological Effects of Cocaine

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Prenatal cocaine administration increases glutathione and alpha-tocopherol oxidation in fetal rat brain

Cited by 42 publications

References 47 publications

Ischemia Enhances Activation by Ca2+and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Ischemia Enhances Activation by Ca2+and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Age-related changes in glutathione and glutathione-related enzymes in rat brain

Role of Mitochondria on the Neurological Effects of Cocaine

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Product

Resources

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Ischemia Enhances Activation by Ca²⁺and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex

Ischemia Enhances Activation by Ca²⁺and Redox Modification of Ryanodine Receptor Channels from Rat Brain Cortex