Higher sensitivity to cadmium induced cell death of basal forebrain cholinergic neurons: A cholinesterase dependent mechanism

Pino, Javier del; Zeballos, Garbriela; Anadón, M.J.; Capo, Miguel Andrés; Díaz, María Jesús Villamide; Moyano, Paula; Frejo, María Teresa

doi:10.1016/j.tox.2014.09.004

Cited by 43 publications

(21 citation statements)

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“…This result is consistent with that of previous studies that showed that acute administration of cadmium had depressogenic effects and decreased locomotor activity [30, 31]. In addition, cadmium decreases cognitive functions in humans [32] and induces neuronal death in basal forebrain cholinergic neurons [33]. Furthermore, cadmium treatment facilitates an increase in the number and size of senile plaques and promotes memory impairments [34].…”

Section: Discussionsupporting

confidence: 92%

Dendropanax morbifera Léveille extract ameliorates cadmium-induced impairment in memory and hippocampal neurogenesis in rats

Kim

Yim

Yoo

et al. 2016

BMC Complement Altern Med

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BackgroundCadmium leads to learning and memory impairment. Dendropanax morbifera Léveille stem extract (DMS) reduces cadmium-induced oxidative stress in the hippocampus. We investigated the effects of DMS on cadmium-induced impairments in memory in rats.MethodsCadmium (2 mg/kg), with or without DMS (100 mg/kg), was orally administered to 7-week-old Sprague-Dawley rats for 28 days. Galantamine (5 mg/kg), an acetylcholinesterase inhibitor, was intraperitoneally administered as a positive control. A novel-object recognition test was conducted 2 h after the final administration. Cell proliferation and neuroblast differentiation were assessed by immunohistochemistry for Ki67 and doublecortin, respectively. Acetylcholinesterase activity in the synaptosomes of the hippocampus was also measured based on the formation of 5,5′-dithio-bis-acid nitrobenzoic acid.ResultsAn increase in the preferential exploration time of new objects was observed in both vehicle-treated and cadmium-treated rats. In addition, DMS administration increased cell proliferation and neuroblast differentiation in the dentate gyrus of vehicle-treated and cadmium-treated rats. Acetylcholinesterase activity in the hippocampal synaptosomes was also significantly higher in the DMS-treated group than in the vehicle-treated group. The effect of DMS on cadmium-induced memory impairment and cell proliferation in the hippocampus was comparable to that of galantamine.ConclusionsThese results suggest that DMS ameliorates cadmium-induced memory impairment via increase in cell proliferation, neuroblast differentiation, and acetylcholinesterase activity in the hippocampus. The consumption of DMS may reduce cadmium-induced neurotoxicity in animals or humans.

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Section: Discussionsupporting

confidence: 92%

Dendropanax morbifera Léveille extract ameliorates cadmium-induced impairment in memory and hippocampal neurogenesis in rats

Kim

Yim

Yoo

et al. 2016

BMC Complement Altern Med

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“…[ 1 2 3 ] To a great extent, some toxic heavy metals are known to be concentrated in the food chain, Cd among them, and which is not degradable; consequently, it is easily transported from soil to plants, which animals and humans largely depend on for survival. [ 4 ]…”

Section: Introductionmentioning

confidence: 99%

“…Upon exposure, regardless of the route, Cd elicits its deleterious effects by impeding cellular energy metabolism; it disrupts calcium actions, generates free radicals, and causes alterations in antioxidant defense mechanisms, thereby inducing oxidative stress and damage, which affect cellular machinery involving such as proteins, DNA, and lipids. [ 4 5 ] In the recent years, the prevalence of cardiovascular diseases has been on the increase globally, accounting for major causes of morbidity and mortality. [ 6 ] Because the cardiovascular system is not the primary target of Cd toxicity, the exact influence of the metal on the cardiovascular system remains controversial.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective and antioxidant influence of aqueous extracts from Sesamum indicum seeds on oxidative stress induced by cadmium in wistar rats

et al. 2016

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Background:Oxidative stress has been implicated in the pathogenesis of several acute and chronic diseases of the heart as a result of indiscriminate exposure to cardiotoxic heavy metals. The study reported here was designed to evaluate the possible ameliorative effect of aqueous extracts from Sesamum indicum (SI) seeds on oxidative stress induced by cadmium (Cd) in Wistar rats.Materials and Methods:Daily administration of Cd (200 mg/L Cd as CdCl2) in the animals’ main drinking water for 21 days led to oxidative stress. Thereafter, the ameliorative effects were assessed by measuring biochemical parameters such as extent of lipid peroxidation (LPO), lipid profile, and enzymatic and nonenzymatic antioxidants, as well as serum aminotransferase activities.Results:Treatment with SI extract elicited notable reduction in serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels as well as concomitant increase in high-density lipoprotein cholesterol. SI extract also reversed the elevations witnessed in serum aminotransferase activities, LPO level, and ameliorated enzymatic and nonenzymatic antioxidant status in the heart of Cd-exposed rats.Conclusion:Thus, SI appears to be an attractive candidate with potential for the novel treatment of cardiotoxicity and management of oxidative stress arising from Cd exposure.SUMMARY Cadmium (200 mg/L) exposure in drinking water caused pronounced oxidative stress and cardiac tissue damage in animal modelAqueous extract of Sesamum indicum (SI) seeds at a dose of 200 or 400 mg/kg body weight exhibited a significant reversal effect in all biochemical parameters measured such as extent of lipid peroxidation, lipid profile, and enzymatic and nonenzymatic antioxidants, as well as serum aminotransferase activitiesAqueous extract of SI seeds possess antioxidant and cardioprotective potential in a dose-dependent manner, thus conferring protection against oxidative stress induced by cadmium. Abbreviation used: SI: Sesamum indicum, Cd: Cadmium, CdCl2: Cadmium chloride, LPO: Lipid peroxidation, TBA: Thiobarbituric acid, ALT: Alanine aminotransferase, AST: Aspartate aminotransferase, ALP: Alkaline phosphatise, TC: Total cholesterol, TG: Triglyceride, HDL-C: Highdensity lipoprotein cholesterol, LDL-C: Low-density lipoprotein cholesterol, SD: Standard deviation, GSH: Glutathione, SOD: Superoxide dismutase, CAT: Catalase, GST: Glutathione-S-transferase, GPx: Glutathione peroxidise.

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“…The higher chronic exposure occurs in mines and industrial workers such as smelting, battery manufacturing and pigment production or residents of cadmium-polluted areas close to these industries. Moreover, it has been identified that cadmium level in miners chronically exposed to it reached levels up to 6.2 μmol/ L in the brain [36]. Besides, it has been described that bloodbrain barrier (BBB) is not fully developed in young animals [37].…”

Section: Discussionmentioning

confidence: 99%

“…For this reason, higher cadmium concentrations can reach the brain more easily than in adults. Though no data is available, the reports showed that acute exposure can also occur following large doses as an occupational hazard or by accidental leakage of cadmium-containing batteries, the doses from 10 to 100 μmol/L of cadmium concentrations would be relevant for acute high level exposure [36].…”

Section: Discussionmentioning

confidence: 99%

Autophagy Plays a Cytoprotective Role During Cadmium-Induced Oxidative Damage in Primary Neuronal Cultures

Wang

Song

et al. 2015

Biol Trace Elem Res

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Cadmium (Cd) induces significant oxidative damage in cells. Recently, it was reported that autophagy could be induced by Cd in neurons. However, little is known about the role of reactive oxygen species (ROS) during Cd-induced autophagy. In our study, we examined the cross-talk between ROS and autophagy by using N-acetyl cysteine (NAC, an antioxidant) and chloroquine (CQ, a pharmacological inhibitor of autophagy) in a primary rat neuronal cell cultures. We observed accumulation of acidic vesicular organelles and the increased expression of endogenous protein light chain 3 (LC3) in Cd-treated neurons, revealing that Cd induced a high level of autophagy. Moreover, increased levels of ROS were observed in neurons treated with Cd, showing that ROS accumulation was closely associated with neuron's exposure to Cd. Furthermore, we found that autophagy was inhibited by using CQ and/or NAC with further aggravation of mitochondrial damage, lactate dehydrogenase (LDH) leakage and hypoploid apoptotic cell number in Cd-treated neurons. These results proved that autophagy has a cytoprotective role during Cd-induced toxicity in neurons, and it can prevent the oxidative damage. These findings may enable the development of novel therapeutic strategies for neurological diseases.

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Higher sensitivity to cadmium induced cell death of basal forebrain cholinergic neurons: A cholinesterase dependent mechanism

Cited by 43 publications

References 71 publications

Dendropanax morbifera Léveille extract ameliorates cadmium-induced impairment in memory and hippocampal neurogenesis in rats

Dendropanax morbifera Léveille extract ameliorates cadmium-induced impairment in memory and hippocampal neurogenesis in rats

Cardioprotective and antioxidant influence of aqueous extracts from Sesamum indicum seeds on oxidative stress induced by cadmium in wistar rats

Autophagy Plays a Cytoprotective Role During Cadmium-Induced Oxidative Damage in Primary Neuronal Cultures

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