A Proposed Concept Model for Cancer Risk in Nigerian Electronic Waste Exposure - A Brief Report.

Aim: This report aims to render a proposed concept model for cancer risk in Nigerian electronic waste exposure by making deductions from data on the assessment of Nigerians' exposure to toxic metals in e-waste, using biomarkers of exposure and genotoxicity to evaluate the risk of cancer development. Material and methods: In the cross-sectional study, 632 consenting participants, consisting of 381 e-waste workers (EW) and 120 environmental e-waste exposed participants (EEEP), age-matched with 131 unexposed participants (controls), were enrolled from Benin, Lagos and Ibadan, Southwestern Nigeria. Levels of selected toxic metals in blood and essential metals in serum were determined using inductively coupled plasma-mass spectrometry. Oxidative stress biomarkers, including malondialdehyde and uric acid (UA), and activities of enzymatic antioxidants [catalase, superoxide dismutase (SOD), γ-glutamyltransferase (GGT) and glutathione peroxidase (GPx)], were determined in serum using standard methods like spectrophotometry. Genotoxicity biomarkers - wild-type tumour suppressor protein (wt-p53), 8-oxoguanine-DNA glycosylase (OGG1), and 8-hydroxy-2'-deoxyguanosine (8-OHdG); glutathione (GSH); and tumour markers [prostate-specific antigen (PSA) and alpha-fetoprotein] - were determined in serum using ELISA. Micronucleus assay was carried out using microscopy. Data were analysed using ANOVA and Pearson's correlation coefficient at α0.05. Results: There was evidence indicating elevated levels of genotoxic toxic metals, decreased levels of genome protective metals, increased oxidative stress markers as well as reduced cellular antioxidants in both EW and EEEP compared to controls. Additionally, the levels of wt-p53 in EW and EEEP were lower than controls, while OGG1 activity in EEEP was higher. The PSA and alpha-fetoprotein in EW were more elevated than EEEP and controls, respectively. The MnPCE/1000PCE in EW was higher than EEEP and controls. Conclusion: The proposed schematic model could be adopted to illustrate cancer risk in Nigerian population exposed to electronic waste.

Clofibrate, a PPAR-α agonist, abrogates sodium fluoride-induced neuroinflammation, oxidative stress, and motor incoordination via modulation of GFAP/Iba-1/anti-calbindin signaling pathways.

Fluoride is an environmental contaminant that is ubiquitously present in air, water, and soil. It is commonly added in minute quantity to drinking water, toothpaste, and mouth rinses to prevent tooth decay. Epidemiological findings have demonstrated that exposure to fluoride induced neurodevelopmental toxicity, developmental neurotoxicity, and motor disorders. The neuroprotective effect of clofibrate, a peroxisome proliferator-activated receptor alpha agonist, was investigated in the present study. Forty male Wistar rats were used for this study and randomly grouped into 10 rats per group as control, sodium fluoride (NaF) alone (300 ppm), NaF plus clofibrate (250 mg/kg), and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. NaF was administered in drinking water while clofibrate and lisinopril were administered by oral gavage. Markers of neuronal inflammation and oxidative stress, acetylcholinesterase activity, and neurobehavioral (hanging wire and open field) tests were performed. Immunohistochemistry was performed on brain tissues, and they were probed with glial fibrillary acidic protein, ionized calcium-binding adaptor molecule 1, and cerebellar Ca2+ -binding protein calbindin-D28k. The results showed that NaF significantly increased of oxidative stress and neuroinflammation and inhibited AChE activity. Immunostaining showed reactive astrocytes, microgliosis, loss of dendritic spines, and arborization in Purkinje cells in rats administered only NaF. Neurobehavioral results showed that cotreatment of NaF with clofibrate improved muscular strength and locomotion, reduced anxiety, and significantly reduced astrocytic count. Overall, cotreatment of NaF with either clofibrate or lisinopril showed neuroprotective effects by mitigating neuronal inflammation and oxidative and motor incoordination. Hence, clofibrate could be seen as a novel drug candidate against neurodegeneration and motor disorders.

Gallic acid protects against bisphenol A-induced alterations in the cardio-renal system of Wistar rats through the antioxidant defense mechanism.

Bisphenol A (BPA) is a small molecular weight endocrine disrupting chemical (EDC) that is used in the production of plastics with deleterious effects on various body systems while gallic acid (GA) is a known antioxidant capable of ameliorating EDC-induced perturbations. In this study, adult male rats (180 ± 5 g) were divided into four groups of eight rats each: Group A (Control rats): 0.2 ml of corn oil; Group B (GA-treated rats): 20 mg/kg/day GA (dissolved in distilled water); Group C (BPA-treated rats): 10 mg/kg/day BPA suspended in 0.2 ml corn oil; Group D (BPA + GA-treated rats): BPA (10 mg/kg/day) with a concomitant GA (20 mg/kg/day). All treatments were orally administered for 14 days. BPA induced significant decrease in systolic, diastolic and mean arterial blood pressure while causing a significant (p < 0.05) increase in heart rate in the rats. It significantly (p < 0.05) raised both renal and cardiac reactive oxygen species and depleted the antioxidant system. There were also significant (p < 0.05) increases in serum myeloperoxidase, nitric oxide, urea and creatinine in the BPA-treated rats. Lesions of the heart and kidney including inflammation, vascular congestion and erosion of epithelial cells were also observed in the BPA-treated rats. However, the concomitant treatment with GA ameliorated all the BPA-induced alterations of the cardio-renal system. Hence, low dose of GA serves a protective function against BPA-induced toxicity of the heart and kidney.

Low doses of multi-walled carbon nanotubes elicit hepatotoxicity in rats with markers of oxidative stress and induction of pro-inflammatory cytokines.

The investigation into the potential health risks associated with the use of engineered nanoparticles is a major scientific interest in recent years. The present study elucidated the involvement of pro-inflammatory cytokines, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in carboxylated multi-walled carbon nanotubes (MWCNTs)-induced hepatotoxicity. Pubertal rats were exposed to purified MWCNTs at 0, 0.25, 0.50, 0.75 and 1.0 mg/kg for 5 consecutive days. Results indicated that exposure to MWCNTs caused liver damage evidenced by significant elevation in serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT) when compared with control. Moreover, MWCNTs significantly decreased superoxide dismutase (SOD) and glutathione S-transferase (GST) activities as well as glutathione level whereas it significantly increased catalase (CAT) and glutathione peroxidase (GPx) activities in liver of the treated rats. Moreover, the dose-dependent increase in hepatic hydrogen peroxide (H2O2) and lipid peroxidation levels were accompanied by marked increase in micronucleated polychromatic erythrocytes (MNPCE) in the MWCNTs-treated rats. Administration of MWCNTs significantly increased serum concentrations of pro-inflammatory cytokines namely interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in the treated rats. Immunohistochemical analysis showed significantly increased COX-2 and iNOS protein expressions in the liver of MWCNTs-treated rats. In conclusion, carboxylated MWCNTs induces hepatic damage via disruption of antioxidant defense systems, promotion of pro-inflammatory cytokines generation and expression of COX-2 and i-NOS in rats.

Ameliorative effect of gallic acid on doxorubicin-induced cardiac dysfunction in rats.

BACKGROUND: The use of doxorubicin (DOX) as an antineoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. METHODS: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A-F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days. RESULTS: The exposure of rats to DOX led to a significant (p<0.05) decrease in the cardiac antioxidant defence system and elevation of creatine kinase myocardial band and lactate dehydrogenase. The electrocardiography results showed a significant decrease in heart rate, QRS, and QT-segment prolongation. GA alone improved the antioxidant defence system. CONCLUSIONS: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxidant status and prevented cardiac damage.