Article Neuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus Mehmet Kanter 1 , Cuneyt Unsal 2 , Cevat Aktas 3 and Mustafa Erboga 3 Abstract The purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd þ QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dis- mutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Admin- istration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd þ QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improve- ment in neurodegeneration of hippocampus after Cd exposure in rats. Keywords Cadmium, Quercetin, hippocampus, oxidative stress, neuronal damage Introduction The main threats to human health from toxic metals are associated with exposure to lead, cadmium (Cd), mercury, and arsenic. Cd is a ubiquitous environ- mental and industrial pollutant that accumulates in animals and humans (Waisberg et al., 2003). The sources of human exposure to Cd include primary metal industries, production of certain batteries, intake of contaminated food or water, and inhalation of tobacco smoke or polluted air (Lo ´ pez et al., 2006; Nawrot et al., 2006). The targets for Cd toxicity include the kidney, lung, gastrointestinal tract, bone, and also the central nervous system (CNS) (Lehman and Klaassen, 1986; Nordberg, 1984; Webster and Valois, 1981). Although it is diffi- cult for foreign substances to cross the blood–brain bar- rier (BBB), after chronic low-level exposure, Cd may affect the integrity or permeability of the barrier and reach the CNS (Murphy, 1997; Shukla et al., 1996). Numerous animal studies have demonstrated beha- vioral disorders, morphological, and biochemical changes in the CNS in Cd-exposed experimental ani- mals (De Castro et al., 1996; Webster and Valois, 1981). In clinical and epidemiological studies, 1 Department of Histology and Embryology, Faculty of Medicine, Istanbul Medeniyet University, Istanbul, Turkey 2 Department of Psychiatry, Faculty of Medicine, Namik Kemal University, Tekirdag, Turkey 3 Department of Histology and Embryology, Faculty of Medicine, Namik Kemal University, Tekirdag, Turkey Corresponding author: Mehmet Kanter, Department of Histology and Embryology, Faculty of Medicine, Istanbul Medeniyet University, Istanbul 34710, Turkey. Email: mkanter65@yahoo.com Toxicology and Industrial Health 1–10 © The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0748233713504810 tih.sagepub.com at Namik Kemal Universitesi on August 19, 2015 tih.sagepub.com Downloaded from