Selenium and zinc supplementation mitigates metals-(loids) mixture- mediated cardiopulmonary toxicity via attenuation of antioxidant, anti-inflammatory and antiapoptotic mechanisms in female Sprague Dawley rats.

This study evaluated the cardiopulmonary protective effects of essential elements (Zn and Se) against heavy metals mixture (HMM) exposure. Twenty five female Sprague Dawley albino rats, divided in to five groups: controls were orally treated only with distilled water; next, group 2 was exposed to HMM with the following concentrations: 20 mg/kg of Pb body weight, 0.40 mg/kg of Hg, 0.56 mg/kg of Mn, and 35 mg/kg of Al. Groups 3, 4 and 5 were exposed to HMM and co-treated with zinc chloride (ZnCl2; 0.80 mg/kg), sodium selenite (Na2SeO3;1.50 mg/kg) and both zinc chloride and sodium selenite, respectively. The experiment lasted for 60 days. Afterwards animals were sacrificed, and we conduced biochemical and histopathological examination of the heart and lungs. HMM only exposed animals had an increased levels of malondialdehyde (MDA) and nitric oxide (NO), increased IL-6 and TNF-α, attenuated SOD, GPx, CAT and GSH and caspase 3 in the heart and lungs. HMM affected NF-kB and Nrf2 in the heart muscle with histomorphological alterations. Zn and Se attenuated adverse effects of HMM exposure. Essential element supplementation ameliorated heavy metal cardiopulmonary intoxication in rats.

Engaging One Health in Heavy Metal Pollution in Some Selected Nigerian Niger Delta Cities. A Systematic Review of Pervasiveness, Bioaccumulation and Subduing Environmental Health Challenges.

The Niger Delta environment is under serious threat due to heavy metal pollution. Many studies have been conducted on the heavy metal contamination in soils, water, seafood and plants in the Niger Delta ecosystem. However, there is a lack of clear understanding of the health consequences for people and strategies for attaining One Health, and a dispersion of information that is accessible. The study focused on investigating the contamination levels, distributions, risks, sources and impacts of heavy metals in selected regions of the Niger Delta. Prior studies revealed that the levels of certain heavy metals, including Cd, Pb, Cu, Cr, Mn, Fe and Ni, in water, sediment, fish and plants in most Niger Delta ecosystems were higher than the acceptable threshold attributed to various anthropogenic stressors. In the reviewed Niger Delta states, ecosystems in Rivers state showed the highest concentrations of heavy metals in most sampled sites. Groundwater quality was recorded at concentrations higher than 0.3 mg/L World Health Organization drinking water guideline. High concentrations of copper (147.915 mg/L) and zinc (10.878 mg/L) were found in Rivers State. The heavy metals concentrations were greater in bottom-dwelling organisms such as bivalves, gastropods and shrimp than in other fishery species. Heavy metal exposure in the region poses risks of communicable and non-communicable diseases. Diverse remediation methods are crucial to reduce contamination levels, but comprehensive strategies and international cooperation are essential to address the health hazards. Actively reducing heavy metals in the environment can achieve One Health objectives and mitigate disease and economic burdens.

Selenium and zinc alleviate hepatotoxicity induced by heavy metal mixture (cadmium, mercury, lead and arsenic) via attenuation of inflammo-oxidant pathways.

Heavy metals (HM) are believed to be injurious to humans. Man is exposed to them on daily basis unknowingly, with no acceptable protocol to manage its deleterious effects. These metals occur as mixture of chemicals with varying concentrations in our atmosphere. There are growing calls for the use of essential metals in mitigating the injurious effects induced by heavy metals exposure to man; therefore, the aim of this study was to evaluate the protective effects of essential metals (Zinc and Selenium) in a mixture of heavy metal toxicity. In this study, except for negative controls, all other groups were treated with lead (PbCl2 , 20 mg kg-1 ); cadmium (CdCl2 , 1.61 mg kg-1 ); mercury (HgCl2 , 0.40 mg kg-1 ), and arsenic (NaAsO3, 10 mg kg-1 ) that were formed in distilled water. Pb, Cd, As, and Hg were administered as mixtures to 35, 6 weeks old rats weighing between 80 to 100 g for 60 days. Group I served as normal control without treatment, group II positive control received HM mixture, while groups III to V received HMM with Zn, Se, and Zn + Se respectively. Animal and liver weights, HM accumulation in the liver, food intake (FI), water intake (WI), liver function test, malondialdehyde (MDA), and inflammatory/transcription factor/apoptosis markers were checked. Also, antioxidant enzymes, and histological studies were carried out. Metal mixture accumulated in the liver and caused toxicities which were ameliorated by Zn and Se administration. HM caused significant decrease in FI, WI and distorted the level of liver enzymes, lipid peroxidation, inflammatory markers, antioxidants and architecture of the liver. Co administration with Zn or Se or both reversed the distortions. This study lays credence to the evolving research on the public health implications of low dose metal mixtures and the possible ameliorative properties of Zn and Se.

Ameliorative Effects of Zn and Se Supplementation on Heavy Metal Mixture Burden via Increased Renal Metal Excretion and Restoration of Redoxo-Inflammatory Alterations.

Heavy metals (HM)in the environment have provoked global attention because of its deleterious effects. This study evaluated the protection offered by Zn or Se or both against HMM-induced alterations in the kidney. Male Sprague Dawley rats were distributed into 5 groups of 7 rats each. Group I served as normal control with unrestricted access to food and water. Group II received Cd, Pb, and As (HMM) per oral daily for 60 days while groups III and IV received HMM in addition to Zn and Se respectively for 60 days. Group V received both Zn and Se in addition to HMM for 60 days. Metal accumulation in feces was assayed at days 0, 30, and 60 while accumulation in the kidney and kidney weight were measured at day 60. Kidney function tests, NO, MDA, SOD, catalase, GSH, GPx, NO, IL-6, NF-Κb, TNFα, caspase 3, and histology were assessed. There is a significant increase in urea, creatinine, and bicarbonate ions while potassium ions decreased. There was significant increase in renal function biomarkers, MDA, NO, NF-Κb, TNFα, caspase 3, and IL-6 while SOD, catalase, GSH, and GPx decrease. Administration of HMM distorted the integrity of the rat kidney, and co-treatment with Zn or Se or both offered reasonable protection suggesting that Zn or Se could be used as an antidot against the deleterious effects of these metals.

Selenium and zinc protect against heavy metal mixture-induced, olfactory bulb and hippocampal damage by augmenting antioxidant capacity and activation of Nrf2-Hmox-1 signaling in male rats.

PURPOSE/AIM OF THE STUDY: Heavy metals and metalloids have been implicated in neurodenerative diseases. Present study has evaluated the potential protective effects of Se and Zn on heavy metals and metalloids mixture-induced (Cd, Pb, Hg and As) toxicity in the hippocampus and olfactory bulb in male rats. MATERIALS AND METHODS: Five groups of Wistar rats were randomly divided in to: controls, toxic metals mixture (TMM) exposed rats (PbCl2, 20 mg·kg-1; CdCl2, 1.61 mg·kg-1; HgCl2, 0.40 mg·kg-1 and NaAsO3, 10 mg·kg-1)), TMM + Zn, TMM + Se and TMM-+Zn + Se groups and were orally treated for 60 days. RESULTS: We found that in hippocampus and olfactory bulb, TMM generated increased lipid peroxidation and diminished antioxidant capacity. These adverse effects induced by TMM were alleviated by Zn and Se co-treatment; moreover, essential trace elements (Zn and Se) decreased activity of acetylcholinesterase, reduced Cd, Pb, Hg and As bioaccumulation in hippocampus and olfactory bulb and decreased levels of TNF-α in the hippocampus. TMM treated rats had lower levels of Hmox-1 (hippocampus), higher levels of Nrf2 (olfactory bulb and hippocampus) and NF-kB (olfactory bulb). TMM treated rats showed significantly highest time in locating the escape hole. Histopathological examination revealed hypertrophied granule cells in OB of TMM exposed rats. CONCLUSION: Zn and Se supplementation can reverse quaternary mixture-induced (Cd, Pb, Hg and As) toxicity in hippocampus and OB in male albino rats.

An Update Overview on Mechanistic Data and Biomarker Levels in Cobalt and Chromium-Induced Neurodegenerative Diseases.

There is increasing evidence that the imbalance of metals as cobalt (Co) and chromium (Cr) may increase the risk of development and progression of neurodegenerative diseases (NDDs). The human exposure to Co and Cr is derived mostly from industry, orthopedic implants, and polluted environments. Neurological effects of Co and Cr include memory deficit, olfactory dysfunction, spatial disorientation, motor neuron disease, and brain cancer. Mechanisms of Co and Cr neurotoxicity included DNA damage and genomic instability, epigenetic changes, mitochondrial disturbance, lipid peroxidation, oxidative stress, inflammation, and apoptosis. This paper seeks to overview the Co and Cr sources, the mechanisms by which these metals induce NDDs, and their levels in fluids of the general population and patients affected by NDDs. To this end, evidence of Co and Cr unbalance in the human body, mechanistic data, and neurological symptoms were collected using in vivo mammalian studies and human samples.

Ni and Al mixture amplifies cerebellar oxido-inflammatory responses, down regulates AChE and BDNF/NGF levels in motor impairment in male albino rats.

BACKGROUND: Aluminum and nickel are potent neurotoxicants to which humans are constantly exposed. Previous studies have demonstrated that these two metals can affect the motor system, but their effects on the cerebellum, a central nervous system region with the highest number of neurons, have remained largely unexplored. Therefore, we conducted a study to investigate the adverse effects of Al, Ni, and Al+Ni in vivo. METHODS: In our study, seven male Sprague Dawley rats per group were orally exposed to deionized water, 0.2 mg/kg of Ni, 1 mg/kg of Al, and 0.2 mg/kg of Ni + 1 mg/kg of Al (as a binary heavy metals mixture; HMM), respectively. RESULTS: Ni, Al, and HMM exposed rats accumulated higher levels of Al and Ni compared to controls, and HMM treated animals had higher levels of Ca and Fe in the cerebellum (p < 0.05). Malondialdehyde (MDA) levels were significantly (p < 0.05) higher in the HMM, Ni, and Al treated groups compared to the control group that received deionized water. Superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx) activities were significantly (p < 0.05) reduced in the HMM, Ni, and Al treated groups compared to the control group that received deionized water. Ni, Al, and HMM significantly (p < 0.05) shortened the length of time of the grip in comparison to the control. Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) levels were significantly decreased in the nickel, Al, and heavy metal mixture groups compared with the control group. Moreover, there was a significant decrease in the activity of acetylcholinesterase (AChE) and a increase in cyclooxygenase-2 (COX-2) activity in the Ni, Al, and HMM treated groups compared to the control group. CONCLUSION: HMM exposed animals had significantly poorer performance in the Rotarod test (p < 0.05) than controls. Al and Ni induced impairment of cerebellar function at various levels.

Nickel and aluminium mixture elicit memory impairment by activation of oxidative stress, COX-2, and diminution of AChE, BDNF and NGF levels in cerebral cortex and hippocampus of male albino rats.

This study evaluated nickel and aluminium-induced neurotoxicity, as a binary metal mixture. Twenty-eight male Sprague Dawley albino rats were weight-matched and divided into four groups. Group 1 (control) received deionized water. Group 2 and 3 received Aluminium (1 mg/kg) and Nickel (0.2 mg/kg) respectively, while Group 4 received Ni and Al mixture HMM three times a week orally for 90 days. Barnes maze tests was performed. Rats were sacrificed under pentobarbital anaesthesia, cerebral cortex and hippocampus were separated, and metal levels were measured using Atomic Absorption Spectroscopy (AAS). Malondialdehyde (MDA), catalase (CAT), glutathione content (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), Brain Derived Neurotrophic Factor (BDNF), Nerve growth factor NGF, cyclo-oxygenase COX-2 and Acetylcholinesterase (AChE) were assayed using ELISA kits. Ni/Al binary mixture exposed rats showed a shorter latency period (though not significant) of 3.21 ± 1.40 s in comparison to 3.77 ± 1.11 (Ni only) and 3.99 ± 1.16(Al only). Ni/Al mixture gp had the lowest levels of Mg in both the hippocampus and frontal cortex when compared with the individual metals. In the hippocampus Al only exposed rats significantly showed p < 0.05 higher iron and Ca levels in comparison to Ni/Al mixture. Al alone significantly showed p < 0.05 lower levels of Fe but higher Ca than the Ni/Al mixture group. Exposure to Al only showed lower levels of BDNF in comparison to Ni/Al combination, whereas Ni/Al mixture gp had lower levels of NGF in comparison to the individual metals in the hippocampus. In the frontal cortex Ni only, group showed significantly lower BDNF in comparison to Ni/Al mixture whereas the mixture showed significantly lower NGF when compared with Al only group. There were higher levels of COX-2 in the Ni/Al mixture than individual metal treated rats in both hippocampus and frontal cortex. AChE levels in the Ni/Al mixture group was higher than Ni or Al only gps in the hippocampus whereas in the frontal cortex, Ni/Al exposed rats showed significantly lower AChE levels in comparison to Al only group. Ni, Al and Ni/Al mixture exhibited memory impairment by activation of oxidative stress, COX-2, and diminution of AChE, BDNF and NGF levels in cerebral cortex and hippocampus. The BDNF-COX-2 AChE signalling pathway may be involved in the neurotoxicity of Ni and Al.

Trace Element Concentrations in Autopsied Heart Tissues from Patients with Secondary Cardiomyopathy.

Cardiomyopathies (CMP) represent a significant health problem as they have a poor long-term prognosis and often require transplantation. Heavy metals are known to have cardiotoxic effects and some of them, such as cadmium (Cd), are found to be elevated in the urine and blood of individuals with heart diseases; nevertheless, direct measurement of metals (e.g. zinc (Zn) which is necessary for normal heart function), in the myocardium of individuals with CMP has not been performed. Here, we aimed to analyze the levels of a group of metals in the myocardium of the left ventricle in individuals with CMP. At the Institute of Pathology, we collected 52 samples of left ventricle post-mortem, out of which 19 subjects had been diagnosed with CMP (mean age: 72 y ± 10), and 33 subjects had not suffered from any heart disease (mean age: 67 y ± 15). We found out that individuals with CMP had a significantly higher concentrations of lead, nickel, manganese and copper than non-CMP subjects (p = 0.002, p < 0.001, p = 0.011, and p = 0.002). Interestingly, zinc was significantly lower in CMP subjects than in n-CMP individuals (p = 0.017). Our results indicated the involvement of an increased lead, nickel, copper and manganese heart load in individuals with CMP coupled with lower concentrations of zinc.

Non-Uniform Bioaccumulation of Lead and Arsenic in Two Remote Regions of the Human Heart's Left Ventricle: A Post-Mortem Study.

The extent of heavy-metal-induced cardiotoxicity is proportional to the levels of metal bioaccumulation, and it was previously assumed that heavy metals accumulate uniformly in the myocardium. Therefore, the aim of this study was to investigate concentrations of metals and metalloids in two distant regions of the left ventricle (LV), the base of the LV, and apex of the LV using inductively coupled plasma mass spectrometry (ICP-MS). We also examined the potential correlation between metal levels and the thickness of the interventricular septum in twenty LV specimens (ten from the base of LV and ten from the apex of LV) from 10 individuals (mean age 75 ± 6 years). We found significantly higher concentrations of arsenic and lead in the LV apex compared to the base of the LV. We also found a positive correlation between the concentrations of arsenic in the myocardium of LV and the thickness of the interventricular septum. Our results indicate that arsenic and lead accumulate to a higher extent in the apex of the LV compared to the base of the LV. Therefore, future studies designed to measure levels of metals in heart muscle should consider non-uniform accumulation of metals in the myocardium.

Zinc and selenium attenuate quaternary heavy metal mixture-induced testicular damage via amplification of the antioxidant system, reduction in metal accumulation, inflammatory and apoptotic biomarkers.

Heavy metals (HMs) such as cadmium (Cd), lead (Pb), arsenic (As), and mercury (Hg) are highly toxic elements. They are often found together in nature as a heavy metal mixture (HMM) and are known to contribute to subfertility/infertility as environmental pollutants. This study aims to evaluate the potential benefits of treating HMM-induced testicular pathophysiology with zinc (Zn) and/or selenium (Se). Six-week-old male Sprague Dawley rats were grouped into 5 (n = 7). The control group received deionized water, while the other groups were treated with PbCl2 (20 mg kg-1), CdCl2 (1.61 mg kg-1), HgCl2 (0.40 mg kg-1), and Na2AsO3 (10 mg kg-1) in deionized water for 60 days. Additionally, groups III to V received Zn, Se, and Zn/Se, respectively, for 60 days. The study evaluated testis weight, metal accumulation, sperm analysis, FSH, LH, testosterone, prolactin, oxidative stress, antioxidants, pro-inflammatory and apoptotic markers, and presented structural changes in the testis as micrographs. HMM caused a significant increase in testis weight, metal accumulation, prolactin, oxidative stress, and pro-inflammatory and apoptotic markers, while significantly decreasing semen analysis, FSH, LH, and testosterone. Histology showed decreased spermatogenesis and spermiogenesis, as evidenced by the structure of the germ cells and spermatids. However, Zn, Se, or both ameliorated and reversed some of the observed damages. This study provides further evidence for the mitigative potential of Zn, Se, or both in reversing the damage inflicted by HMM in the testis, and as a countermeasure towards improving HM-induced decrease in public health fecundity.

Polycyclic Aromatic Hydrocarbons in Soil and Vegetation of Niger Delta, Nigeria: Ecological Risk Assessment.

The Niger Delta, Nigeria, is noted for crude oil exploration. Whereas there seems to be a handful of data on soil polycyclic aromatic hydrocarbon (PAH) levels in this area, there is a paucity of studies that have evaluated soil and vegetation PAHs simultaneously. The present study has addressed this information gap. Fresh Panicum maximum (Jacq) (guinea grass), Pennisetum purpureum Schumach (elephant grass), Zea mays (L.) (maize), and soil samples were collected in triplicate from Choba, Khana, Trans-Amadi, Eleme, Uyo, and Yenagoa. PAHs determination was carried out using GC-MS. The percentage composition of the molecular weight distribution of PAHs, the molecular ratio of selected PAHs for identification of possible sources, and the isomeric ratio and total index of soil were evaluated. Pennisetum purpureum Schumach (elephant grass) from Uyo has the highest (10.0 mg·kg-1) PAH while Panicum maximum (Jacq) (guinea grass) has the highest PAH (32.5 mg·kg-1 from Khana. Zea mays (L.) (maize) from Uyo (46.04%), Pennisetum purpureum Schumach (elephant grass) from Trans-Amadi (47.7%), guinea grass from Eleme (49.2%), and elephant grass from Choba (39.9%) contained the highest percentage of high molecular weight (HMW) PAHs. Soil samples from Yenagoa (53.5%) and Khana (55.3%) showed the highest percentage of HMW PAHs. The total index ranged 0.27-12.4 in Uyo, 0.29-8.69 in Choba, 0.02-10.1 in Khana, 0.01-5.53 in Yenagoa, 0.21-9.52 in Eleme, and 0.13-8.96 in Trans-Amadi. The presence of HMW PAHs and molecular diagnostic ratios suggest PAH pollution from pyrogenic and petrogenic sources. Some soils in the Niger Delta show RQ(NCs) values higher than 800 and require remediation to forestall ecohealth consequences.

Selenium and zinc alleviate quaternary metal mixture -induced neurotoxicity in rats by inhibiting oxidative damage and modulating the expressions of NF-kB and Nrf2/Hmox-1 pathway.

Background: This study evaluated the potential protective effects of Zn and Se in the cerebellum and cerebral cortex, two fundamentally important brain regions, in albino rats that were exposed to heavy metals mixture (Al, Pb, Hg and Mn). Methods: Animals were divided into five groups of seven animals per group with following patterns of exposure, controls group 1 were orally treated with deionized water for 60 days; group 2 was exposed to heavy metal mixture (HMM) with following concentrations (20 mg·kg-1 of Pb body weight; 0.40 mg·kg-1 of Hg; 0.56 mg·kg-1 of Mn; and 35 mg·kg-1; of Al), while groups 3,4 and 5 were exposed to HMM and orally co-treated with zinc chloride (ZnCl2; 0.80 mg/kg), sodium selenite (Na2SeO3;1.50 mg/kg) and zinc chloride plus sodium selenite (ZnCl0.2 + Na2SeO3) respectively. Results: Exposure to HMM depressed cellular antioxidant apparatus, induced generation of lipid peroxidation markers (Malondialdehyde and NO), downregulated expression of transcription factors (Nrf2, and NF-kB) and upregulated Caspase 3 levels. HMM potentiated acetylcholinesterase activity and induced moderate histopathological alterations. Nevertheless, Zn, Se and in particular Zn + Se had recovering effects on all mentioned hazardous effects produced by HMM exposure in the cerebral cortex and cerebellum. Conclusions: Selenium and zinc exert neuroprotection via Nrf2/NF-kB signaling pathways against quaternary heavy metal mixture-induced impairments in albino Sprague Dawley rats.

Heavy metals and inflammatory, oxidative/antioxidant and DNA damage biomarkers among people living with HIV/AIDS (PLWHA) in Niger Delta, Nigeria.

This study evaluated the association of heavy metals (HMs) and effect biomarkers (inflammation, oxidative stress/antioxidant capacity and DNA damage) among people living with HIV/AIDS (PHWHA) in Niger Delta area, Nigeria. Blood levels of lead (BPb), cadmium (BCd), copper (BCu), zinc (BZn), iron (BFe), C-reactive protein (CRP), Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α), Interferon-γ (IFN-γ), Malondialdehyde (MDA), Glutathione (GSH) and 8-hydroxy-2-deoxyguanosine (8-OHdG) were determined in a total of 185 participants, 104 HIV-positive and 81 HIV-negative sampled in both Niger Delta and non-Niger Delta regions. BCd (p < 0.001) and BPb (p = 0.139) were higher in HIV-positive subjects compared to HIV-negative controls; on the contrary, BCu, BZn and BFe levels were lower (p < 0.001) in HIV-positive subjects compared to HIV-negative controls. The Niger Delta population had higher levels of heavy metals (p < 0.01) compared to non-Niger Delta residents. CRP and 8-OHdG were higher (p < 0.001) in HIV-positive than in HIV-negative subjects and in Niger-Delta than in non-Niger Delta residents. BCu had significant positive dose-response relationship with CRP (61.9%, p = 0.063) and GSH (1.64%, p = 0.035) levels in HIV-positive subjects, and negative response with MDA levels (26.6%, p < 0.001). Periodic assessment of HMs levels among PLWHA is recommended.

Local and Systemic Hypoxia as Inductors of Increased Aluminum and Iron Brain Accumulation Promoting the Onset of Alzheimer's Disease.

Human environment is highly contaminated with aluminum, and aluminum is toxic to majority of tissues, particularly to neurons. In previous decades, aluminum exposure was frequently linked with the onset of Alzheimer's disease (AD), and increased levels of Al were detected in the brains of individuals with AD. People who live in a certain area are exposed to aluminum in a similar way (they eat the same vegetable and other foodstuffs, use similar cosmetics, and buy medications from the same manufacturer), nevertheless not all of them develop Alzheimer's disease. Majority of known risk factors for AD promote atherosclerosis and consequently reduce brain blood supply. In this review, we highlighted the significance of local (carotid disease and atherosclerosis of intracranial blood vessels) and systemic hypoxia (chronic obstructive pulmonary disease and anemia) in the development of AD. Nerve tissue is very sophisticated and sensitive to hypoxia and aluminum toxicity. As a side effect of compensatory mechanisms in case of hypoxia, neurons start to uptake aluminum and iron to a greater extent. This makes perfect a background for the gradual onset and development of AD.

Immune System and Epidemics: The Role of African Indigenous Bioactive Substances.

With over 6 million coronavirus pandemic deaths, the African continent reported the lowest death rate despite having a high disease burden. The African community's resilience to the pandemic has been attributed to climate and weather conditions, herd immunity, repeated exposure to infectious organisms that help stimulate the immune system, and a disproportionately large youth population. In addition, functional foods, herbal remedies, and dietary supplements contain micronutrients and bioactive compounds that can help boost the immune system. This review identified significant traditional fermented foods and herbal remedies available within the African continent with the potential to boost the immune system in epidemics and pandemics. Methodology: Databases, such as PubMed, the Web of Science, and Scopus, were searched using relevant search terms to identify traditional African fermented foods and medicinal plants with immune-boosting or antiviral capabilities. Cereal-based fermented foods, meat-, and fish-based fermented foods, and dairy-based fermented foods containing antioxidants, immunomodulatory effects, probiotics, vitamins, and peptides were identified and discussed. In addition, nine herbal remedies and spices belonging to eight plant families have antioxidant, immunomodulatory, anti-inflammatory, neuroprotective, hepatoprotective, cardioprotective, and antiviral properties. Peptides, flavonoids, alkaloids, sterols, ascorbic acid, minerals, vitamins, and saponins are some of the bioactive compounds in the remedies. Bioactive compounds in food and plants significantly support the immune system and help increase resistance against infectious diseases. The variety of food and medicinal plants found on the African continent could play an essential role in providing community resilience against infectious diseases during epidemics and pandemics. The African continent should investigate nutritional, herbal, and environmental factors that support healthy living and longevity.

Essential Trace Elements Prevent the Impairment in the Retention Memory, Cerebral Cortex, and Cerebellum Damage in Male Rats Exposed to Quaternary Metal Mixture by Up-regulation, of Heme Oxygynase-1 and Down-regulation of Nuclear Factor Erythroid 2-related Factor 2-NOs Signaling Pathways.

In the present study, we examined adverse effects of metals and metalloids in the Cerebral cortex (CC) and Cerebellum (CE). Group 1 comprised from the controls while other four groups of male Wistar rats were treated with following pattern: Group II (Heavy Metal Mixture HMM only: PbCl2, 20 mg·kg-1; CdCl2, 1.61 mg·kg-1; HgCl2, 0.40 mg·kg-1, and NaAsO3,10 mg·kg-1), Groups III (HMM + ZnCl2); Group IV (HMM + Na2SeO3) and Group V (HMM + ZnCl2 + Na2SeO3) for 60 days per os. HMM promoted oxidative stress in the CC and CE of treated rats compared to controls; moreover, exposure to HMM led to increased activity of the AChE and pro-inflammatory cytokines; also, HMM promoted accumulation of caspase 3 and other transcriptional factors such as Nrf2 and decreased levels of Hmox-1. Essential metals reduced increased bioaccumulation of Pb, Cd, As and Hg in CC and CE caused by HMM exposure. Also, all mentioned adverse effects were diminished by essential metals treatment (Se and Zn). HMM exposed rats had considerably less escape dormancy than controls. Histopathological analysis revealed moderate cell loss at the intermediate (Purkinje cell) and granular layer. Zinc and selenium supplementations could reverse adverse effects of heavy metals at various cellular levels in neurons.

Zn and Se abrogate heavy metal mixture induced ovarian and thyroid oxido-inflammatory effects mediated by activation of NRF2-HMOX-1 in female albino rats.

The thyroid is vital for the proper functioning of the female reproductive system since it regulates the metabolism and development of ovary. This is an evaluation of the essential trace elements ETE on the heavy metals mixture HMM mediated oxido-inflammatory effects in the ovary and thyroid of female albino rats. Eight groups (5 female rats /group) were treated as follows for 60 days: Group 1: Deionized water only; Group 2: (Pb, Hg, Mn and Al); Group 3: HMM + ZnCl2, 0.80 mg/kg; Group 4: HMM + Na2SeO3, 1.50 mg/kg; Group 5: HMM + ZnCl2, 0.80 mg/kg and Na2SeO3, 1.50 mg/kg combined. On day 60 animals were euthanized, ovary and thyroid were harvested and used for, MDA, NO, antioxidants, TNF-α, IL-6, HMOX-1, Caspase-3, NF-KB, NRF2, HM and histopathology. There was significant bioaccumulation of Pb, Al, Hg and MN; elevated IL-6 and TNF-α, MDA and NO, caspase-3 and NRF2, NFKB and HMOX-1 with significant decrease in antioxidants in the HMM only group in comparison to the control. Co-treatment with ETE reversed most of these effects. ETE may ameliorate HMM -induced ovarian and thyrotoxicity in female albino rats by blunting oxido-inflammatory activities.

Potential deleterious effects of paracetamol dose regime used in Nigeria versus that of the United States of America.

Paracetamol, also known as acetaminophen (N-acetyl-para-aminophenol, APAP) is the world's most used over-the-counter analgesic-antipyretic drug. Despite its good safety profile, acetaminophen can cause severe hepatotoxicity in overdose, and poisoning from paracetamol has become a major public health concern. Paracetamol is now the major cause of acute liver failure in the United States and Europe. This systematic review aims at examining the likelihood of paracetamol use in Nigeria causing more liver toxicity vis-à-vis the reduced maximum recommended daily adult dose of 3 g for the 500 mg tablet. Online searches were conducted in the databases of PubMed, Google Scholar and MEDLINE for publications using terms like "paracetamol toxicity," "acetaminophen and liver toxicity," "paracetamol and liver diseases in Nigeria," and other variants. Further search of related references in PubMed was carried out, and synthesis of all studies included in this review finalized. There were 94 studies that met the inclusion criteria. Evaluation of hepatic disorder was predicated mostly on a constellation of clinical features and limited clinical laboratory investigations. Determination of blood paracetamol concentration was rarely reported, thus excluding paracetamol poisoning as one of the likely causes of liver disorders in Nigeria. In Nigeria and elsewhere, several factors are known to increase paracetamol's predisposition to liver injury. They include: the over-the-counter status of paracetamol, use of fixed-dose combinations of paracetamol with other drugs, malnutrition, dose miscalculations, and chronic alcohol consumption. The tendency to exceed the new paracetamol maximum daily dose of 3 g in Nigeria may increase its risk for hepatotoxicity than observed in the United States of America known for emphasizing lower dose of the drug. In addition to recommending the new maximal daily paracetamol dose allowance, the historical maximum daily adult dose of 4 g should be de-emphasized in Nigeria.

Zinc and selenium mitigated heavy metals mixture (Pb, Al, Hg and Mn) mediated hepatic-nephropathy via modulation of oxido-inflammatory status and NF­kB signaling in female albino rats.

This study evaluated the protective role o of zinc and selenium on heavy metal mixture (HMM) induced hepatic-nephropathy. Twenty-five female Wistar albino rats were weight-matched and divided into five groups of five female rats each. Group 1(control) received deionized water only. Group 2 received heavy metal mixture HMM (20 mg·kg-1 of Pb, 0.40 mg·kg-1 of Hg, 0.56 mg·kg-1 of Mn and 35 mg·kg-1 of Al). Groups 3, 4 and 5 were co-administered with metal mixtures and Zn, Se and Zn + Se respectively. Treatments were through oral gavage for 60 days; animals were sacrificed under pentobarbital and liver and kidney harvested for tests. Zn, Se and Zn + Se reduced metal accumulation in the liver and kidney. HMM exposure caused non-significant increase in AST, ALP, ALT and TP, but significant increase in IL-6 and TNF -α, Nf-kB, Hmox-1, Nfr2, MDA and NO when compared to the control. Essential trace elements significantly decreased IL-6 and TNF -α, Nf-kB, Hmox-1and Nfr2 in comparison to HMM only group. Treatment with Zn, Se and Zn + Se significantly reversed the HHM mediated decreased SOD levels. HMM triggered degenerative changes in the central vein, showed vacuolations with connective tissues fragmentation and lymphocytes infiltration were reversed by essential trace elements. Essential trace elements supplementation is protective against HMM mediated hepato-renal impairment.