Carcinogenic and non-carcinogenic risk assessment of consuming metal-laden wild mushrooms in Nigeria: Analyses from field based and systematic review studies.

This study investigated the potential health risk associated with the consumption of metal-laden mushrooms in Nigeria. Concentrations of Pb, Cd, Cr, Cu, Ni, Zn and Al in wild mushrooms collected from the Nigerian environment were measured using atomic absorption spectrometer. Also, systematic analysis of articles on metal accumulation in mushrooms from Nigeria were obtained from scientific databases. Using hazard model indices, the metal concentration in mushrooms were evaluated for their potential carcinogenic and non-carcinogenic health risk when consumed by adults and children. Zn and Cd, respectively, had the highest and lowest mean concentrations (mg kg-1) in the analysed mushrooms from the field study, while Fe and Co, respectively, had the highest and lowest mean concentrations (mg kg-1) in the systematically reviewed articles. In the field study, the percentage distribution of THQ of the heavy metals greater than 1 was 0% and 42.85% for adults and children respectively. While for the systematic study, 30% and 50% of the heavy metals for adults and children respectively exceeded the limit of 1. The hazard indices obtained from both the systematic and field studies for both age groups were all >1, indicating significant health risk. The findings from both the systematic and field studies revealed that consuming metal-laden mushrooms by adults and children increases the carcinogenic risk to Cd, Cr, and Ni since they exceeded the acceptable limit of 1E-04 stated by USEPA guideline. Based on the findings from the systematic and field studies, it suggests that consuming mushrooms collected from metal polluted substrates increases carcinogenic and non-carcinogenic health risk among Nigerians.

Mitochondrial dysfunctions elicited by solid waste leachates provide insights into mechanisms of leachates induced cell death and pathophysiological disorders.

Emissions (mainly leachates and landfill gases) from solid waste facilities are laden with mixtures of dangerous xenobiotics implicated with significant increase in various pathophysiological disorders including cancer, and eventual mortality of exposed wildlife and humans. However, the molecular mechanisms of solid waste leachates induce pathophysiological disorders and cell death are still largely unknown. Although, evolving evidence implicated generation of reactive oxygen species and oxidative stress as the possible mechanism. Recent scientific reports are linking reactive oxygen species and mitochondrial dysfunctions as the player mechanism in pathophysiological disorder and apoptosis induced by xenobiotics in solid waste leachates. This systematic review presents an explicit discussion of recent scientific findings on the structural and functional alterations in mitochondria induced by solid waste leachates as the molecular mechanisms plausibly responsible for the pathophysiological disorders, cancer and cell death reported in landfill toxicology and epidemiological studies. This review aims to increase scientific understanding on solid waste leachate induced mitochondria dysfunctions as the key player in molecular mechanisms of solid waste induced toxicity. The findings in this review were mainly from using primary cells, cell lines, Drosophila and fish. Whether the findings will similarly be observed in mammalian test systems in vivo and particularly in exposed humans, remained to be investigated. Improvement in technological advancements, enforcement of legislation and regulations, and creation of sophisticated health surveillance against exposure to solid waste leachates, will expectedly mitigate human exposure to solid waste emissions and contamination of the environment.

Landfill soil leachates from Nigeria and India induced DNA damage and alterations in genes associated with apoptosis in Jurkat cell.

Landfill soil leachates, containing myriad of xenobiotics, increase genotoxic and cytotoxic stress-induced cell death. However, the underlying mechanism involved in the elimination of the damaged cells is yet to be fully elucidated. This study investigated the apoptotic processes induced in lymphoma (Jurkat) cells by landfill soil leachates from Olusosun (OSL, Nigeria) and Nagpur (NPL, India). Jurkat was incubated with sub-lethal concentrations of OSL and NPL for 24 h and analyzed for DNA fragmentation and apoptosis using agarose gel electrophoresis and Hoechst 33258-PI staining, respectively. Complementary DNA expression profiling of some pro-apoptotic and anti-apoptotic genes regulating apoptosis was also analyzed using real-time PCR (RT-PCR) method. Agarose gel electrophoresis revealed DNA fragmentations in OSL and NPL-treated cells. Hoecsht-33258 - Propidium Iodide (PI) based apoptotic analysis confirmed apoptotic cell death in exposed Jurkat. RT-PCR analysis revealed different fold changes in the pro- and anti-apoptotic genes in OSL and NPL-treated Jurkat. There was significant increase in fold change of the up-regulated genes; apoptosis inducing factor mitochondrion-associated 2 (AIFM2), Fas-associated death domain (FADD), Caspase-2, Caspase-6, BH3 interacting domain death agonist (BID), tumor suppressor (p53), and BCL2 associated agonist of cell death (BAD) and down-regulation of apoptosis inhibitor 5 (API5). Results suggest that OSL and NPL elicited genotoxic stress-related apoptosis in Jurkat. The dysregulation in the expression of genes involved in apoptotic processes in wildlife and human exposed to landfill emissions may increase aetiology of various pathological diseases including cancer.

Plastic pollution threat in Africa: current status and implications for aquatic ecosystem health.

Rapid population growth and poor waste management practice are among the main drivers of plastic pollution in modern times, thus making Africa a hotspot for plastic pollution both now and in the future. This study is a review of plastic pollution reports from the African aquatic environment with regard to causes, current status, toxicological implications and implications for ecosystem services. A total of 59 plastic pollution studies from 1987 to September 2020 were reviewed. They comprised 15 from North Africa (NA) (Algeria, Egypt, Morocco and Tunisia), six from East Africa (EA) (Ethiopia, Kenya, Tanzania and Uganda), 13 from West Africa (WA) (Ghana, Guinea-Bissau, Mauritania and Nigeria), and 25 studies from Southern Africa (SA) (South Africa). This shows that plastic pollution studies in Africa, according to the sub-regions, are in the order: SA > NA > WA > EA. High human population in the basins of African large aquatic systems is identified as the greatest driver enhancing plastic surge in the aquatic environment. The occurrence of plastics was mostly reported in the estuarine/marine environment (42 studies) compared to the freshwater environment (only 17 studies). Plastics have also been reported in the three compartments of the aquatic environment: water column, benthic sediment and animals. Zooplankton, annelids, molluscs, insects, fishes and birds were reported as bioindicators of plastic ingestion in the inland and coastal waters of Africa. Polyethylene, polyethylene terephthalate (polyester) and polypropylene were the common plastic polymers observed in the African aquatic environment. In situ toxicological implications of the ingested plastic polymers were not reported in any of the studies. However, reports from laboratory-controlled experiments showed that these polymers are deleterious to aquatic animal health. More research efforts need to delineate the plastic pollution status of the East, West and North of Africa. Furthermore, such studies are required to identify the plastic polymers and in situ ecotoxicological impacts of plastics on both animal and human health.

Bioactivity and modulatory functions of Napoleona vogelii on oxidative stress-induced micronuclei and apoptotic biomarkers in mice.

Napoleona vogelii is used in traditional medicine for the management of pain, inflammatory conditions and cancer. This study was conducted to investigate the modulatory mechanisms of methanol stem bark extract of N. vogelii on induction of micronuclei, apoptotic biomarkers and in vivo antioxidant enzymes in mice. Forty male albino mice were randomly divided into eight groups (n = 5) and were administered distilled water (DW, 5 mL/kg) as negative control, 100, 200 or 400 mg/kg of the extract respectively for 28 days before the injection of cyclophosphamide (CP, 40 mg/kg) i.p. on the 28th day. The remaining groups were administered 100, 200 or 400 mg/kg of the extract only for 28 days. Twenty four hours after injection of CP or administration of the last dose of extract, animals were euthanized by cervical dislocation and blood samples collected for determination of in vivo antioxidants, the spleen harvested for immunohistochemical expression of NFκB, Bcl-2, Bax and p53. Bone marrow smears were also made for the micronucleus assay. Treatment with the extract resulted in a significant (p < 0.0001) reduction in frequency of micronucleated polychromatic erythrocytes (MNPCEs) compared to CP exposed control conferring protection of 75.09, 94.74 and 96.84% at 100, 200 or 400 mg/kg respectively. In extract and CP exposed animals, there were significant (p < 0.05) increases in GSH, GST and SOD with a corresponding significant (p < 0.05) reduction in MDA. In addition, the extract significantly downregulated cytoplasmic levels of NFκB and Bcl-2 and upregulated Bax and p53. These findings demonstrate that N. vogelli may serve as an interesting lead for chemo-preventive drug development.

Genetic and systemic toxicity induced by silver and copper oxide nanoparticles, and their mixture in Clarias gariepinus (Burchell, 1822).

Unanticipated increase in the use of silver (Ag) and copper oxide (CuO) nanoparticles (NPs) due to their antimicrobial properties is eliciting environmental health concern because of their coexistence in the aquatic environment. Therefore, we investigated the genetic and systemic toxicity of the individual NPs and their mixture (1:1) using the piscine micronucleus (MN) assay, haematological, histopathological (skin, gills and liver) and hepatic oxidative stress analyses [malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT)] in the African mud catfish, Clarias gariepinus. The fish were exposed to sublethal concentrations (6.25-100.00 mg/L) of each NP and their mixture for 28 days. Both NPs and their mixture induced significant (p < 0.05) increase in MN frequency and other nuclear abnormalities. There was significant decrease in haemoglobin concentration, red and white blood cell counts. Histopathological lesions observed include epidermal skin cells and gill lamellae hyperplasia and necrosis of hepatocytes. The levels of MDA, GSH and activities of SOD and CAT were impacted in C. gariepinus liver following the exposure to the NPs and their mixture. Interaction factor analysis of data indicates antagonistic genotoxicity and oxidative damage of the NPs mixture. These results suggest cytogenotoxic effects of Ag NPs, CuO NPs and their mixture via oxidative stress in Clarias gariepinus.

Evaluation of cytogenotoxicity and oxidative stress parameters in male Swiss mice co-exposed to titanium dioxide and zinc oxide nanoparticles.

A number of studies have investigated the adverse toxic effects of titanium dioxide (TiO2) nanoparticles (NPs) or zinc oxide (ZnO) NPs. Information on the potential genotoxic effects of the interactions of TiO2 NPs and ZnO NPs in vivo is lacking. Therefore, this study was designed to investigate the cytogenotoxicity of TiO2 NPs or ZnO NPs alone or their mixtures using the bone marrow micronucleus assay, and mechanism of damage through the evaluation of oxidative stress parameters in the liver and kidney tissues of Swiss mice. Intraperitoneal administration of doses between 9.38 and 150.00 mg/kg of TiO2 NPs or ZnO NPs or TiO2 NPs + ZnO NPs was performed for 5 and 10 days, respectively. TiO2 NPs alone induced a significant (P <  0.05) increase in micronucleated (Mn) polychromatic erythrocytes (PCEs) at the applied doses compared with the negative controls, with a significant difference between 5 and 10 days for TiO2 NPs alone and TiO2 NPs + ZnO NPs. Concurrently, TiO2 NPs alone for 5 days and TiO2 NPs and TiO2 NPs + ZnO NPs for 10 days significantly (P <  0.05) decreased the percentage PCE: normochromatic erythrocyte (NCE) indicating cytotoxicity; with a significant difference between the two periods. Significant (P <  0.001) changes in the activities of superoxide dismutase (SOD) and catalase (CAT), and levels of reduced glutathione (GSH) and malondialdehyde (MDA) were observed in the liver and kidney of mice exposed to TiO2 NPs or ZnO NPs alone or their mixtures. These results suggest that TiO2 NPs alone was genotoxic; TiO2 NPs and TiO2 NPs + ZnO NPs were noticeably cytotoxic while ZnO NPs was not cytogenotoxic. The individual NPs or their mixtures induced oxidative stress.

Chemical characterization of simulated landfill soil leachates from Nigeria and India and their cytotoxicity and DNA damage inductions on three human cell lines.

Landfill soils are sources of emerging carcinogens, teratogens and mutagens in the environment. There is inadequate information on its possible health risk and cytogenotoxicity. This study evaluated chemical characterization of four simulated landfill leachates with their cytotoxicity and DNA damage in human cells. Hepatocarcinoma (HepG2), lymphoma (Jurkat) and osteosarcoma (HOS) cells, incubated with 6.25, 12.5, 25, 50, 75 and 100% of Aba Eku (AEL), Olusosun (OSL), Awotan (AWL) and Nagpur (NPL) simulated leachates for 24 h, were assessed for cell viability using MTT assay and morphological alterations. DNA damage was also assessed after 24 h treatment of cells with sub-lethal concentrations of the leachates using comet assay. Metals and organic compounds in the soil leachates were determined using inductively coupled plasma-mass spectrometry (ICP-MS) and gas chromatography-mass spectroscopy (GC-MS) respectively. The leachates induced significant cytotoxicity in the treated cells with evidence of apoptosis; shrunken morphologies, detachment from the substratum and cytoplasmic vacuolations. Similarly, there was significant DNA damage induced in the treated cells, with increased Olive tail moment, tail length and % tail DNA. Jurkat was the most sensitive (Jurkat > HepG2 > HOS) to the cytotoxic and genotoxic effects of the leachates. All the analyzed metals except Cd, Fe, Zn and Mn were found at levels lower than standard allowable limits. 32, 17, 23 and 23 different PAHs and PCBs were detected in AEL, AWL, OSL and NPL respectively, at varying retention peak times. These toxic constituents induced the observed cytogenotoxicity in the cells and may suggest possible public health risk.

Genotoxicity and cytotoxicity of chromium, copper, manganese and lead, and their mixture in WIL2-NS human B lymphoblastoid cells is enhanced by folate depletion.

Heavy metal exposure or dietary deficiency is associated with increased genetic damage, cancer and age-related diseases. Folate (vitamin B9) required for DNA repair and synthesis may increase cellular susceptibility to metal induced genotoxicity. This study investigated the interactive effects of folic acid deficiency and sufficiency on genome instability and cytotoxicity induced by chromium (VI), copper (II), manganese (II), lead (IV), and their mixture (CCMP) in WIL2-NS human B lymphoblastoid cells. WIL2-NS cells were cultured in folic acid deficient (20 nM) and replete (2000 nM) RPMI 1640 medium treated with different concentrations (0.00-1000 µM) of the metals and CCMP for 48 h. Chromosomal damage and cytotoxicity were measured using the Cytokinesis-block Micronucleus Cytome assay. CCMP, Cr, Pb, Cu and Mn induced concentration dependent, increases in cells with chromosome damage (micronuclei, nucleoplasmic bridges, nuclear buds) and necrotic cells and decreased nuclear division index. The metals exhibited different cytotoxic and genotoxic potentials (CCMP>Cr>Pb>Cu>Mn) in both folate deficient and sufficient cells, with the cytogenotoxic effects being greater in folate deficient cells. Significant interaction between the metals and folic acid suggests that folic acid deficiency exacerbated cell proliferation inhibition and genome instability induced by metals. Folate deficiency, increasing metal concentration, and their interactions explained 3-11%, 74-92% and 4-12% of the variance of DNA damage biomarkers. In conclusion, exposure to the tested metals (0.01-1000 µM) increased chromosomal DNA damage in WIL2-NS cells and this was exacerbated by folate deficiency.