Impaired Energy Metabolism after Co-Exposure to Leadand Ethanol

Verma, Suresh; Dua, Raina; Gill, Kiran Dip

doi:10.1111/j.1742-7843.2005.pto_11.x

Cited by 10 publications

(3 citation statements)

References 26 publications

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“…Both animal experiments and human surveys on the effect of Pb exposure on MDA and GSH revealed an increase in MDA and a decrease in the GSH in blood and brain. 46 – 48 A similar result was observed on the effect of lead on GSH and MDA levels in our experiment. In addition, the activity of CAT, SOD, and GST was also reduced in the brain of rats following lead exposure as observed in the report of other researchers.…”

Section: Discussionsupporting

confidence: 88%

Trévo abrogates Lead Acetate Neurotoxicity in Male Wistar Rats viz Antiamyloidogenesis, Antiglutaminergic, and Anticholinesterase Activities

Ilesanmi

Odewale

Avwioroko

et al. 2022

Annals of Neurosciences

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Background: Exposure to lead has been linked to biochemical changes similar to those patients suffering from Alzheimer’s disease. Trévo is a phytonutrient-rich product with antiaging and antioxidant properties. Purpose: To investigate the neuroprotective activity of trévo against lead-induced biochemical changes in male Wistar rats. Methods: The study involves 35 animals that were randomly divided into five groups of seven rats each. Group I (Control): Orally administered distilled water; Group II (Induced): Administered 15 mg/kg of lead acetate (PbA) intraperitoneally; Group III (Treatment group): Orally administered 2 mL/kg of trévo for two days before co-administration with PbA for 12 consecutive days; Group IV (Treatment group): Orally administered 5 mL/kg of trévo for two days prior to coadministration with PbA for 12 consecutive days; Group V: Orally administered 5 mL/kg of trévo for 14 consecutive days. Animals were anesthetized with diether and the brain excised and processed for the following biochemical assays: Malonedialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GT), acetylcholinesterase (AChE), beta-amyloid, glutamate, Na+/K+ ATPase, and glutamate dehydrogenase (GD). Results: PbA caused significant oxidative stress (increased MDA concentration, decreased GSH concentration, suppressed the activity of CAT, SOD), decreased GT activity, increased activity of AChE, increased the concentration of beta-amyloid, and caused glutamate excitotoxicity (increased concentration of glutamate, decreased activity of Na+/K+ ATPase, and GD) in rat brains. Treatment with trévo at the two different doses significantly prevented oxidative damage, beta-amyloid aggregation, glutamate excitotoxicity, and acetylcholine breakdown induced by lead acetate. Conclusion: Our findings added to the reported pharmacological activity of trévo and supported the antiaging potential of trévo.

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Section: Discussionsupporting

confidence: 88%

Trévo abrogates Lead Acetate Neurotoxicity in Male Wistar Rats viz Antiamyloidogenesis, Antiglutaminergic, and Anticholinesterase Activities

Ilesanmi

Odewale

Avwioroko

et al. 2022

Annals of Neurosciences

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“…This notion received further support from our recent observations of lessened cardiac morphological and functional damage with the facilitated clearance of acetaldehyde via mitochondrial aldehyde dehydrogenase (ALDH-2) following acute or chronic ethanol exposure [8], [9]. More interestingly, evidence also depicted a role of energy metabolism in the ethanol-elicited tissue and cell damage as ethanol ingestion has been shown to reduce the level or activity of ATP, cytochrome oxidase, succinate dehydrogenase and NADH dehydrogenase as well as decrease mitochondrial respiratory rate and phosphorylation efficiency in a variety of tissues such as heart, brain and stomach [10], [11], [12]. This is somewhat coordinated with our earlier finding that alcohol dehydrogenase (ADH), which oxidizes ethanol into acetaldehyde, exacerbated mitochondrial dysfunction manifested as loss of mitochondrial membrane potential and accumulation of mitochondrial O 2 − anion [13].…”

Section: Introductionmentioning

confidence: 99%

Involvement of AMPK in Alcohol Dehydrogenase Accentuated Myocardial Dysfunction Following Acute Ethanol Challenge in Mice

2010

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ObjectivesBinge alcohol drinking often triggers myocardial contractile dysfunction although the underlying mechanism is not fully clear. This study was designed to examine the impact of cardiac-specific overexpression of alcohol dehydrogenase (ADH) on ethanol-induced change in cardiac contractile function, intracellular Ca2+ homeostasis, insulin and AMP-dependent kinase (AMPK) signaling.MethodsADH transgenic and wild-type FVB mice were acutely challenged with ethanol (3 g/kg/d, i.p.) for 3 days. Oral glucose tolerance test, cardiac AMP/ATP levels, cardiac contractile function, intracellular Ca2+ handling and AMPK signaling (including ACC and LKB1) were examined.ResultsEthanol exposure led to glucose intolerance, elevated plasma insulin, compromised cardiac contractile and intracellular Ca2+ properties, downregulated protein phosphatase PP2A subunit and PPAR-γ, as well as phosphorylation of AMPK, ACC and LKB1, all of which except plasma insulin were overtly accentuated by ADH transgene. Interestingly, myocardium from ethanol-treated FVB mice displayed enhanced expression of PP2Cα and PGC-1α, decreased insulin receptor expression as well as unchanged expression of Glut4, the response of which was unaffected by ADH. Cardiac AMP-to-ATP ratio was significantly enhanced by ethanol exposure with a more pronounced increase in ADH mice. In addition, the AMPK inhibitor compound C (10 µM) abrogated acute ethanol exposure-elicited cardiomyocyte mechanical dysfunction.ConclusionsIn summary, these data suggest that the ADH transgene exacerbated acute ethanol toxicity-induced myocardial contractile dysfunction, intracellular Ca2+ mishandling and glucose intolerance, indicating a role of ADH in acute ethanol toxicity-induced cardiac dysfunction possibly related to altered cellular fuel AMPK signaling cascade.

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“…Several studies have been performed, examining the co-exposure of lead and alcohol, but the influence of arsenic has been less elucidated. Considering the prevalence of excessive alcohol and arsenic toxicity [19][20][21][22][23], the potential co-exposure, and the impact of both on hippocampal integrity, this study seeks to determine whether alcohol and arsenic combine to exacerbate neurodegeneration, microglial activation, and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice

Sides,

Nelson,

Nwachukwu

et al. 2023

Brain Sciences

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Both excessive alcohol consumption and exposure to high levels of arsenic can lead to neurodegeneration, especially in the hippocampus. Co-exposure to arsenic and alcohol can occur because an individual with an Alcohol Use Disorder (AUD) is exposed to arsenic in their drinking water or food or because of arsenic found directly in alcoholic beverages. This study aims to determine if co-exposure to alcohol and arsenic leads to worse outcomes in neurodegeneration and associated mechanisms that could lead to cell death. To study this, mice were exposed to a 10-day gavage model of alcohol-induced neurodegeneration with varying doses of arsenic (0, 0.005, 2.5, or 10 mg/kg). The following were examined after the last dose of ethanol: (1) microglia activation assessed via immunohistochemical detection of Iba-1, (2) reactive oxygen and nitrogen species (ROS/RNS) using a colorimetric assay, (3) neurodegeneration using Fluoro-Jade® C staining (FJC), and 4) arsenic absorption using ICP-MS. After exposure, there was an additive effect of the highest dose of arsenic (10 mg/kg) in the dentate gyrus of alcohol-induced FJC+ cells. This additional cell loss may have been due to the observed increase in microglial reactivity or increased arsenic absorption following co-exposure to ethanol and arsenic. The data also showed that arsenic caused an increase in CYP2E1 expression and ROS/RNS production in the hippocampus which could have independently contributed to increased neurodegeneration. Altogether, these findings suggest a potential cyclical impact of co-exposure to arsenic and ethanol as ethanol increases arsenic absorption but arsenic also enhances alcohol’s deleterious effects in the CNS.

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Impaired Energy Metabolism after Co-Exposure to Leadand Ethanol

Cited by 10 publications

References 26 publications

Trévo abrogates Lead Acetate Neurotoxicity in Male Wistar Rats viz Antiamyloidogenesis, Antiglutaminergic, and Anticholinesterase Activities

Trévo abrogates Lead Acetate Neurotoxicity in Male Wistar Rats viz Antiamyloidogenesis, Antiglutaminergic, and Anticholinesterase Activities

Involvement of AMPK in Alcohol Dehydrogenase Accentuated Myocardial Dysfunction Following Acute Ethanol Challenge in Mice

The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice

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