Veterinary Surgery & Reproduction

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Has files: YesSubject: search.filters.subject.Cadmium chloride

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    Nigella sativa oil protects against cadmium-induced intestinal toxicity via promotion of anti-inflammatory mechanisms, mucin expression and microbiota integrity
    (Mashhad University of Medical Sciences, Iran, 2021) Akinrinde, A. S.; Adekanmbi, A. O.; Olojo, F. O.
    Objective: This study examined the protective effects of Nigella sativa oil (NSO) on cadmium (Cd)-induced alterations affecting gut morphology and microbiota composition, as well as the involvement of mucus glycoprotein (MUC2) and immune-inflammatory markers (TNFα and IL-2) in the colon of rats. Materials and Methods: Male Wistar rats, randomized into four groups, were treated either with distilled water (control), CdCl2 (100 mg/kg), CdCl2+NSO (1 ml/kg) or NSO alone. After the experiments, faecal samples were processed for microbial culture on various selective media, while intestinal segments were prepared for histopathological examination and immunohistochemistry. The composition of NSO was analyzed using Gas Chromatography-Mass Spectrometry (GC-MS). Results: Oral Cd administration provoked dramatic increases in faecal counts of potentially pathogenic bacteria (Staphylococci, Enterococci, Pseudomonas and Escherichia coli), while decreasing probiotic lactobacilli counts. Cadmium treatment caused down-regulation of colonic MUC2 (p=0.003) and IL-2 (p=0.03), but increased TNFα (p=0.034), along with reduced goblet cell counts and mucus production. Conversely, treatment with NSO significantly improved Lactobacilli counts (p=0.042), while reducing the levels of potentially pathogenic species. In addition, NSO significantly restored colonic expressions of MUC2 (p=0.001), TNFα (p=0.007) and IL-2 (p=0.025) to control levels. GC-MS analysis of NSO revealed the presence of the active ingredient, thymoquinone and a high content of unsaturated fatty acids, including trans-13-octadecenoic acid and oleic acid. Conclusion: This study highlights the intestinal mucus, microbiota and immuno-inflammatory system as important protective targets of NSO against Cd-induced intestinal toxicity.
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    Adverse effects of In-Vitro cadmium exposure on quality and antioxidant enzyme status of Boar Spermatozoa
    (College of Medicine, University of Ibadan, 2014) Akinrinde, A. S.; Ojo, O. O.; Eboh, A. S.; Adedara, I. A.; Farombi, E. O.
    This study was aimed to evaluate the reproductive toxicity of cadmium chloride (CdCl2. 2.5H2O) in Boar spermatozoa in vitro. Boar spermatozoa obtained from the caudal epididymis of freshly slaughtered boars and dispersed in semen incubation medium (containing tris-hydroxymethyl-aminomethane, citric acid and fructose) were incubated at four different concentrations (0, 0.5, 1.0 and 2.0mM) for 3 hours at 370C. Sperm viability, motility and percentage of abnormal spermatozoa were assessed by microscopy every one hour during the 3–hour incubation period, using aliquots from the incubated samples. Samples thus treated with cadmium chloride were centrifuged and the supernatant was used in the assessment of biochemical parameters of oxidative stress including hydrogen peroxide (H2O2), reduced glutathione (GSH) and Lipid peroxidation. The activities of antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), Glutathione peroxidase (GPX) as well as transaminases (ALT and AST) and alkaline phosphatase (ALP) were also assessed. The percentage of motile and viable spermatozoa decreased significantly (p<0.05) after exposure of spermatozoa to CdCl2 in a concentration- and time-dependent manner. Cadmium significantly increased (p<0.05) the levels of H2O2 and malondialdehyde (MDA) in the spermatozoa with significant reductions (p<0.05) in the activities of SOD, GPX, and CAT. Slight but insignificant increase in GSH concentration was accompanied with a slight increase in GST activity. ALT, AST and ALP activities were differentially modified. The results of this study revealed that cadmium chloride caused reductions in sperm motility and viability, induction of oxidative stress and impairment of antioxidant enzyme activities.