The Cd has been recognized as one of the most toxic environmental and industrial pollutants due to its ability to induce disturbances in several organs and tissues following either acute or chronic exposure. This review accounts for the recent evidence on its mechanisms to induce neurotoxicity, the role of the blood-brain barrier, oxidative stress, interference with calcium, and zinc-dependent processes and apoptosis induction as well as the modulatory effect of metallothionein. Discussion about cadmium neurotoxicity is centered on mechanisms of induction of cellular disfunctions. Future investigations must address those neuronal mechanisms in detail in order to understand cadmium-induced neurotoxicity.
"Oxidative stress affects numerous cellular components, such as proteins, DNA and lipids through oxidation reactions . These alterations in structure produce significant changes in cellular function . "
[Show abstract][Hide abstract] ABSTRACT: The present study investigated the effects of quercetin on the impairment of memory and anxiogenic - like behavior induced by cadmium (Cd) exposure. We also investigated possible alterations in acetylcholinesterase (AChE), Na(+),K(+)-ATPase and δ - aminolevulinate dehydratase (δ-ALA-D) activities as well as in oxidative stress parameters in the CNS. Rats were exposed to Cd (2.5mg/Kg) and quercetin (5, 25 or 50mg/Kg) by gavage for 45days. Animals were divided into eight groups (n=10-14): saline/control, saline/Querc 5mg/kg, saline/Querc 25mg/kg, saline/Querc 50mg/kg, Cd/ethanol, Cd/Querc 5mg/kg, Cd/Querc 25mg/kg and Cd/Querc 50mg/kg. Results demonstrated that Cd impaired memory and has anxiogenic effect.Quercetin prevented these harmful effects induced by Cd. AChE activity decreased in cerebral cortex and hippocampus and increased in hypothalamus of Cd-exposed rats. The Na(+),K(+)-ATPase activity decreased in cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin prevented these effects in AChE and Na(+),K(+)-ATPase activities. Reactive oxygen species production, thiobarbituric acid reactive substance levels, protein carbonyl content and double - stranded DNA fractions increased in cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin prevents totally or partially these effects caused by Cd. Total thiols (T-SH), reduced glutathione (GSH), reductase glutathione (GR) activities decreased and glutathione S-transferase (GST) activity increased Cd exposure rats. Co-treatment with quercetin prevented reduction in T-SH, GSH, GR activities and the rise of GST activity. The present findings show that quercetin prevents alterations in oxidative stress parameters as well as AChE and Na(+),K(+)-ATPase activities, consequently preventing memory impairment and anxiogenic-like behavior displayed by Cd exposure. These results may contribute to a better understanding of the neuroprotective role of quercetin, emphasizing the influence of this flavonoid in the diet for human health, possibly preventing brain injury associated with Cd intoxication.
"Cadmium, as one of the most toxic environmental and industrial pollutants, targets several organs and tissues such as kidney (Johri et al. 2010), blood (Kocak and Akcil 2006), bones (Akesson et al. 2006), testis (Thompson and Bannigan 2008), and brain (Okuda et al. 1997; Lopez et al. 2003; Mendez-Armenta and Rios 2007), resulting in nephrotoxicity, immunotoxicity, osteotoxicity, genotoxicity, neurotoxicity, and tumors following either acute or chronic exposure. Current effective therapy for acute Cd-poisoning is mainly utilizing chelating agents to increase the excretion of Cd, but this method is not suitable for long-term exposure to Cd because of the side effects of the chelators (Nordberg 1984; Sinicropi et al. 2010). "
[Show abstract][Hide abstract] ABSTRACT: Cadmium (Cd), a toxic environmental contaminant, induces neurodegenerative diseases. Celastrol, a plant-derived triterpene, has shown neuroprotective effects in various disease models. However, little is known regarding the effect of celastrol on Cd-induced neurotoxicity. Here we show that celastrol protected against Cd-induced apoptotic cell death in neuronal cells. This is supported by the findings that celastrol strikingly attenuated Cd-induced viability reduction, morphological change, nuclear fragmentation and condensation, as well as activation of caspase-3 in neuronal cells. Concurrently, celastrol remarkably blocked Cd-induced phosphorylation of c-Jun N-terminal kinase (JNK), but not extracellular signal-regulated kinases 1/2 (Erk1/2) and p38, in neuronal cells. Inhibition of JNK by SP600125 or overexpression of dominant negative c-Jun potentiated celastrol protection against Cd-induced cell death. Furthermore, pre-treatment with celastrol prevented Cd downregulation of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and activation of Akt/mammalian target of rapamycin (mTOR) signaling in neuronal cells. Overexpression of wild-type PTEN enhanced celastrol inhibition of Cd-activated Akt/mTOR signaling and cell death in neuronal cells. The findings indicate that celastrol prevents Cd-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. Our results strongly suggest that celastrol may be exploited for the prevention of Cd-induced neurodegenerative disorders. This article is protected by copyright. All rights reserved.
Journal of Neurochemistry 10/2013; 128(2). DOI:10.1111/jnc.12474 · 4.28 Impact Factor
"Copper and cadmium are metals, which are highly toxic to aquatic animals (Jezierska and Witeska 2001; Mendez-Armenta and Rios 2007). Cadmium is a xenobiotic and does not play any known metabolic role. "
[Show abstract][Hide abstract] ABSTRACT: The aim of the present study was to evaluate bioaccumulation of metals in various tissues of the freshwater fish Cyprinus carpio L. exposed to cadmium and copper (a xenobiotic and a microelement). The fish were subjected to short-term (3 h, Cd-S and Cu-S) or long-term (4 weeks, Cd-L and Cu-L) exposures to 100 % 96hLC50 or 10 % 96hLC50, respectively. Blood, gill, liver, head and trunk kidney were isolated weekly from 5 fish of each group for 4 weeks (post-short-term exposure and during long-term exposure). Atomic absorption spectrophotometry technique was applied to measure concentrations of metals (Cd and Cu) in fish tissues. Initial concentrations of copper in fish tissues were higher than levels of cadmium. Cadmium and copper levels increased in all tissues of metal-exposed fish. After short-term exposures (at higher concentration) and during long-term exposures (at lower concentration), similar changes in metal concentrations were observed. The values of accumulation factor (ratio of final to initial metal concentration) were higher for cadmium as compared to copper. Comparison of metal levels and accumulation factors in various tissues revealed that cadmium and copper showed very high affinity to head kidney of common carp (higher than to other tissues), but accumulation factors for cadmium in trunk, head kidney and liver were much higher than for copper. The concentrations of copper in organs of Cu-exposed fish increased only slightly and quickly returned to the control level, which shows that fish organism easily buffered metal level. On the other hand, concentrations of cadmium considerably increased and remained elevated for a long time which suggests that activation of mechanisms of sequestration and elimination of cadmium required more time.
Fish Physiology and Biochemistry 06/2013; 40(1). DOI:10.1007/s10695-013-9819-1 · 1.62 Impact Factor
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