Zeolite abrogates cadmium-induced testicular damage in rats: implication of NF-κB/ TNF-α/IL-1β Pathway

Abstract

ABSTRACT Cadmium (Cd) is an environmental pollutant affecting various tissues and organs, including the testis. Many studies demonstrated that Cd toxicity causes testicular impairment through oxidative stress and inflammatory action. Therefore, this study aimed to demonstrate Cd's testicular toxicity and the protective action of zeolite against cadmium's deleterious effects. Adult male rats were given Cd at a dose of 30mg/kg/day for 28 consecutive days with or without zeolite, which was given at a dose of 100mg/kg/day for 28 days. Testis weight, sperm (count, motility, and abnormalities), serum testosterone and luteinizing hormone (LH), testicular enzymes Acid phosphatase (ACP) and Alkaline phosphatase(ALP), inflammatory cytokines Tumor Necrosis Factor Alpha (TNF-α) , interleukin-1beta (IL-1β) , and Nuclear Factor Kappa B (NF-κB) and oxidative stress were evaluated. Herein, we found that cadmium caused alterations in sperm characteristics, sex hormone disturbance, decline in testicular enzymes, elevated malondialdehyde (MDA) contents, decreased glutathione (GSH), increased Nuclear Factor Kappa B (NF-κB) and pro-inflammatory cytokines Tumor Necrosis Factor Alpha (TNF-α) and interleukin-1beta (IL-1β) levels in testis homogenate. In contrast, zeolite significantly amended these deleterious effects, and the potential mechanism involved the downregulation of Nuclear Factor Kappa B (NF-κB), Tumor Necrosis Factor Alpha (TNF-α) and interleukin-1beta (IL-1β), restoring glutathione (GSH) and reducing malondialdehyde (MDA). Also, zeolite was associated with an increased rate of pregnancy. Our data suggested that oxidative stress and inflammation are responsible for Cd-induced testicular injury and co-administration of zeolite exerts a protective effect via NF-κB /TNF-α/IL-1β pathway.