Cadmium and exposure to stress increase aggressive behavior.
ABSTRACT Environmental toxicants and stress influence the health and behavior of people from different parts of the world. In the present study, aggressive behavior was evaluated in rats exposed to cadmium (Cd) for four weeks and subjected to immobilization stress (IS) based on the resident/intruder paradigm. Latency to the first bite (LB), total number of attacks (NA), total duration of attack manifestations (DAM), and a composite aggression score (CAS) were used to assess aggressiveness. Cadmium concentrations in the blood and the brain were determined. We observed that the parameters of aggressiveness were not altered by either Cd or IS when administered separately. However, animals exposed to Cd+IS had increased NA, DAM, and CAS. Cadmium was detected in the blood and the brain after treatment and Cd+IS exposure modified Cd distribution in these tissues. These results suggest that exposure to low levels of Cd associated with stress may lead to increased aggressiveness in rats.
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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.Physiology & Behavior 06/2014; DOI:10.1016/j.physbeh.2014.06.008 · 3.03 Impact Factor
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ABSTRACT: The effect of heavy metal ions, Cd(2+), Hg(2+) and Pb(2+) on taxifolin binding to bovine serum albumin (BSA) has been investigated by spectroscopic methods. The results indicated that the presence of heavy metal ions significantly affected the binding modes and binding affinities of taxifolin to BSA, and the effects depended on the type of heavy metal ions. One binding mode was found for taxifolin with and without Cd(2+), while two binding modes-a weaker one at low concentration and a stronger one at high concentration-were found for taxifolin in the presence of Hg(2+) and Pb(2+). Cd(2+) decreased the binding affinity of taxifolin for BSA by 7.3%; however, Hg(2+) increased the binding affinity of taxifolin for BSA by 13.3% in lower concentration and 33.3% in higher concentration. Pb(2+) decreased the binding affinity of taxifolin for BSA by 28.4% in lower concentration, and increased the binding affinity of taxifolin for BSA by 20.6% in higher concentration. The decreased binding affinity of taxifolin for BSA in the presence of Cd(2+) was mainly because of the existence of competitive binding between taxifolin and Cd(2+). However, the conformational change of BSA may the main reason for the changed binding affinity and binding distance of taxifolin for BSA in the presence of Hg(2+) and Pb(2+).03/2012; 33(2):327-33. DOI:10.1016/j.etap.2011.12.025
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ABSTRACT: This study investigated the cadmium (Cd) intoxication on cognitive, motor and anxiety performance of rats subjected to long-term exposure to diet with Cd salt or with Cd from contaminated potato tubers. Potato plantlets were micropropagated in MS medium and transplanted to plastic trays containing sand. Tubers were collected, planted in sand boxes and cultivated with 0 or 10μM Cd and, after were oven-dried, powder processed and used for diet. Rats were divided into six groups and fed different diets for 5months: control, potato, potato+Cd, 1, 5 or 25mg/kg CdCl(2). Cd exposure increased Cd concentration in brain regions. There was a significant decrease in the step-down latency in Cd-intoxicated rats and, elevated plus maze task revealed an anxiolytic effect in rats fed potato diet per se, and an anxiogenic effect in rats fed 25mg/kg Cd. The brain structures of rats exposed to Cd salt or Cd from tubers showed an increased AChE activity, but Na(+),K(+)-ATPase decreased in cortex, hypothalamus, and cerebellum. Therefore, we suggest an association between the long-term diet of potato tuber and a clear anxiolytic effect. Moreover, we observed an impaired cognition and enhanced anxiety-like behavior displayed by Cd-intoxicated rats coupled with a marked increase of brain Cd concentration, and increase and decrease of AChE and Na(+),K(+)-ATPase activities, respectively.Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 07/2012; 50(10):3709-18. DOI:10.1016/j.fct.2012.07.016 · 2.61 Impact Factor