Abstract
Cadmium (Cd) exposure can induce acute lethal health-related threats to humans since it has an exceptional ability to accumulate in living organisms and cause toxicological effects. Curcumin (Cur) on the other hand has a wide variety of biological activities and several animal studies have suggested for a potential therapeutic or preventive effects against several ailments and infections. To study the effect of Cur on the toxicity of Cd, sixty Swiss-Webster strain male mice were divided into 6 groups of ten each at random. Group-1 served as the na?ve control and received no treatment. Group-2, 3 and 4 were the experimental controls and were administered once a day with a single oral dose of 50% dimethyl sulphoxide (DMSO), Cur (300 mg/kg) or Cd (100 mg/kg) respectively, for 2 weeks. Group-5 and 6 received Cur and Cd in combination once a day orally for 2 weeks except that Cur in a dose of 150 and 300 mg/kg to group 5 and 6 respectively, was administered one hour before Cd (100 mg/kg) administration to both groups. After treatment period, the animals were subjected to behavioral tests and thereafter, the animals were sacrificed for the estimation of neurotransmitters like serotonin (5-HT), dopamine (DA) and it’s metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) as well as oxidative stress enzymes like lipid peroxides in the form of thiobarbituric acid–reactive substances (TBARS) and total glutathione (GSH) in the forebrain tissue. Cd reduced significantly the body weight gain, the locomotor activity, anxiety behavior in the plus maze and the learning capability (cognitive effect) in the shuttle-box test. Biochemical analysis further revealed that Cd exposure significantly altered the brain neurotransmitters and the oxidative stress enzymes. However, administration of Cur along with Cd had an ameliorating effect on all the behavioral and biochemical parameters studied herein and reduced the toxicity of Cd significantly and dose-dependently. Thus, Cur may be beneficial for anxiety, neuromuscular, and cognitive problems and protect from Cd intoxication.
Highlights
Cadmium (Cd) represents one of the most toxic and carcinogenic heavy metal [1]
The animals were subjected to behavioral tests and thereafter, the animals were sacrificed for the estimation of neurotransmitters like serotonin (5-HT), dopamine (DA) and it’s metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) as well as oxidative stress enzymes like lipid peroxides in the form of thiobarbituric acid–reactive substances (TBARS) and total glutathione (GSH) in the forebrain tissue
Elevated Plus-Maze Test The time spent in open arms was significantly (p < 0.001) lower, whereas time spent in enclosed arms was significantly (p < 0.001) higher in animals treated with Cd as compared to controls (Figure 2(a))
Summary
Cadmium (Cd) represents one of the most toxic and carcinogenic heavy metal [1]. It is considered as a serious environmental and industrial pollutant and may represent as a serious health hazard to humans and other animals [2,3,4]. Some important sources of Cd exposure for humans can be emissions from industries of batteries, metal plating, pigments, plastics, toys and alloy, cigarette smoking and through dietary consumption [5,6,7]. Cd is reported to induce the generation of reactive oxygen species (ROS), and this oxidative stress was found to result in mitochondrial dysfunction and apoptosis, both in vivo and in vitro [14,15]. The oxidative damage within the tissues and DNA damages is considered to be an early manifestation of Cd toxicity and carcinogenicity [16,17]
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