Abstract
We examined, in a rat model of moderate environmental human exposure to cadmium (Cd), whether the enhanced intake of zinc (Zn) may protect against Cd-caused destroying the oxidative/antioxidative balance and its consequences in the brain. The intoxication with Cd (5 mg/L, 6 months) weakened the enzymatic (superoxide dismutase, glutathione peroxidase, catalase) and non-enzymatic (total thiol groups, reduced glutathione) antioxidative barrier decreasing the total antioxidative status and increased the concentrations of pro-oxidants (hydrogen peroxide, myeloperoxidase) in this organ and its total oxidative status. These resulted in the development of oxidative stress and oxidative modifications of lipids and proteins. The co-administration of Zn (30 and 60 mg/L enhancing this element intake by 79% and 151%, respectively) importantly protected against Cd accumulation in the brain tissue and this xenobiotic-induced development of oxidative stress and oxidative damage to lipids and proteins. Moreover, this bioelement also prevented Cd-mediated oxidative stress evaluated in the serum. The favorable effect of Zn was caused by its independent action and interaction with Cd. Concluding, the enhancement of Zn intake under oral exposure to Cd may prevent the oxidative/antioxidative imbalance and oxidative stress in the brain and thus protect against injury of cellular macromolecules in the nervous system.
Highlights
Zinc (Zn) is a bioelement playing a very important role in living systems [1,2,3,4]
The present research indicates the protective effect of Zn against disruption of the oxidative/antioxidative balance resulting in the occurrence of the state of oxidative stress and oxidative injury of the basic cellular macromolecules in the brain under moderate repeated exposure to Cd
This study shows that moderate treatment with Cd may disturb the balance between pro- and antioxidants in the nervous system by inhibiting the activities of enzymatic antioxidants (SOD, glutathione peroxidase (GPx), and CAT) and decreasing the concentrations of the non-enzymatic ones (GSH and TSH), as well as increasing pro-oxidants concentrations (H2 O2 and MPO)
Summary
Zinc (Zn) is a bioelement playing a very important role in living systems [1,2,3,4]. This micronutrient is responsible for the proper activity of numerous enzymes (including antioxidative enzymes), growth, differentiation, and metabolism of cells, synthesis of protein and deoxyribonucleic acid (DNA), immunity, wound healing, and many other functions [2,3,4,5].Supplementation with Zn is recommended in the management of a great number of health conditions, such as acrodermatitis enteropathica, Wilson’s disease, common cold, acne, diarrhea, epilepsy, and to support the immune system [1,4,6,7]. Zinc (Zn) is a bioelement playing a very important role in living systems [1,2,3,4]. This micronutrient is responsible for the proper activity of numerous enzymes (including antioxidative enzymes), growth, differentiation, and metabolism of cells, synthesis of protein and deoxyribonucleic acid (DNA), immunity, wound healing, and many other functions [2,3,4,5]. It is important to notice that in the available literature, there are reports on negative health outcomes of excessive supplementation with this element, such as disturbances in the homeostasis of other bioelements, especially copper (Cu), leading to Cu-deficiency anemia, decrease in the activity of Cu-dependent enzymes, and changes in the metabolism of cholesterol [4,6]. Zn plays a critical role in neurodevelopment and both its deficiency and excess are neurotoxic and are involved in the pathogenesis of neurological diseases such as amyotrophic lateral sclerosis, depression, schizophrenia, Parkinson’s disease, and Alzheimer’s disease [5,7]
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