African mesquite elicits neuroprotective activity against quaternary metal mixture -induced olfactory bulb-hippocampal oxido-inflammatory stress via nrf2-hmox-1pathway.

African mesquite AM is widely used as an anti-inflammatory agent in sub-Sahara Africa especially Nigeria. Given its strong anti-inflammatory potency, this study has evaluated the neuroprotective properties of AM in the hippocampus HIP and olfactory bulb OB of rats exposed to Cd, As, Hg, and Pb. Twenty-five albino Sprague Dawley rats were randomly divided into five groups in this experiment. Group 1, the control received only water. Group 2 received heavy metal mixture HMM (PbCl2 (20 mg/kg), CdCl2 (1.61 mg/kg), HgCl2 (0.40 mg/kg), and NaAsO3 (10 mg/kg), for 60 days. Groups 3, 4, and 5 were treated with HMM along with AM at doses of 500, 1000, and 1500 mg/kg, respectively. AM decreased the Cd, As, Hg, and Pb levels in OB and HIP, restored the activities of antioxidants, Hmox-1, reduced the activities of AChE, NRF2 and NFkB and improved histopathology.

Prosopis africana exerts neuroprotective activity against quaternary metal mixture-induced memory impairment mediated by oxido-inflammatory response via Nrf2 pathway.

The beneficial effects of Prosopis africana (PA) on human health have been demonstrated; however, its protective effects against heavy metals (HM) are not yet understood. This study evaluated the potential neuroprotective effects of PA in the cerebral cortex and cerebellum. To accomplish this, we divided 35 albino Sprague Dawley rats into five groups. Group I did not receive either heavy metal mixture (HMM) or PA. Group II received a HMM of PbCl2 (20 mg/kg), CdCl2 (1.61 mg/kg), HgCl2 (0.40 mg/kg), and NaAsO3 (10 mg/kg) orally for a period of two months. Groups III, IV, and V received HMM along with PA at doses of 500, 1000, and 1500 mg/kg, respectively. PA caused decreased levels of HM accumulation in the cerebral cortex and cerebellum and improved performance in the Barnes maze and rotarod tests. PA significantly reduced levels of IL-6 and TNF-α. PA increased concentrations of SOD, CAT, GSH, and Hmox-1 and decreased the activities of AChE and Nrf2. In addition, levels of MDA and NO decreased in groups III, IV, and V, along with an increase in the number of live neurons. In conclusion, PA demonstrates a complex neuroprotective effect with the potential to alleviate various aspects of HM-induced neurotoxicity.

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.

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.

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.

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.

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.

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.

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.

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.

Banana peel ameliorated hepato-renal damage and exerted anti-inflammatory and anti-apoptotic effects in metal mixture mediated hepatic nephropathy by activation of Nrf2/ Hmox-1 and inhibition of Nfkb pathway.

This study evaluated the protective role of banana peel extract (BP) on heavy metal mixture (HMM) mediated hepatorenal toxicity using a rat model. 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 HMM only (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 the same metal mixture with BP at 200, 400 and 800 mg kg-1, respectively. Treatments were through oral gavage for 60 days; animals were sacrificed pentobarbital anesthesia and liver and kidney harvested for test. Thereafter, metal levels, malondialdehyde (MDA) and nitric oxide (NO), catalase (CAT), glutathione content (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GPx), interlukin-6 (IL-6) and tumor necrosis alpha (Tnf-α), caspase-3 (Cas-3), Nuclear factor kappa B (Nfkb), Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (Hmox-1) were assayed. HMM group presented higher levels of metal, IL-6 and Tnf-α, MDA, NO, Nfkb and Hmox-1 in HMM group which were significantly reduced by BP. BP was protective against metal mixture induced histopathological distortions. HMM exposure significantly distorted hepatorenal functions and BP treatment reduced metal bioavailability and abrogated most of these alterations.

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.

Multi-organ protective effect of Costus afer on low concentration toxic metal mixture in albino rats.

Heavy metal mixture can induce multiple organ damage through oxidative stress and inflammatory processes. Dietary intervention using natural antidotes in resource poor countries where classical metal chelators are either not affordable or available can be explored as an alternative means of management of public health effects of chronic heavy metal exposure. The search for natural antidote against the deleterious effects of heavy metals gives the thrust for this study. Thus, the study investigated the effect of aqueous leaf extract of Costus afer on liver, kidney, brain and testis induced by low dose heavy metal mixture (LDHMM) of PbCl2, CdCl2 and HgCl2 of concentrations of 20 mg/kg, 1.61 mg/kg and 0.40 mg/kg, respectively. Five groups of seven rats each (weight-matched) were used. First and second groups received deionized water and heavy metal mixture and served as normal and toxic controls, respectively. Groups 3, 4 and 5 received through oral gavage 750, 1500, 2250 mg/kg of the Costus afer extract respectively, with the metal mixture concurrently. All treatments were four times a week for 90 days (4/week/90 days). Hepatorenal, hormonal, oxidative stress markers, cytokines (interleukin-6 and interleukin-10), and heavy metals (Pb, Cd and Hg) concentrations were assayed. The one-way analysis of variance, agglomerative hierarchical clustering, parallel coordinates plot, principal component analysis and Bray Curtis dissimilarity were used to statistically analyze the data. LDHMM caused significant changes in these organs and however, the plant extract provided a protective effect against these pathological changes. The statistical analysis revealed that the kidney was the most affected organ, followed by the liver, then brain and testis, respectively. Costus afer may be an important nutraceutical in multi-organ deleterious effects of LDHMM following its regulation of oxidative stress markers, inflammatory cytokines and biometal chelation.

Protective Effect of Costus afer Aqueous Leaf Extract (CALE) on Low-Dose Heavy Metal Mixture-Induced Alterations in Serum Lipid Profile and Hematological Parameters of Male Wistar Albino Rats.

The present work investigated the protective effects of Costus afer Ker Gawl. aqueous leaf extract (CALE) on lipid profile and hematological changes induced by exposure to low-dose heavy metal mixture in male albino rats. The experimental animals were divided into six weight matched groups. The normal (group 1) and toxic (group 2) controls received deionized water and metal mixture (20 mg/kg PbCl2, 1.61 mg/kg CdCl2, and 0.40 mg/kg HgCl2), respectively. Test rats in groups 3, 4, and 5 were treated with metal mixture and CALE (750, 1500, and 2250 mg/kg, respectively), and group 6 received metal mixture and ZnCl2. All treatments were administered through oral gavage for 12 weeks. LDHMM caused a marked increase (p < 0.05) in cholesterol, triglyceride, low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL) levels and a decrease in high-density lipoprotein (HDL), percentage body weight gain, and feed and fluid intake. Also, a significant decrease in RBC, Hb, and PCV, a significant increase in WBC, and no significant increase in platelet PLT were observed in the metal mixture-treated group. But in CALE treated groups, their levels were found to attain almost normal values as found in normal control which is also similar to the zinc-treated group. Costus afer may hold a promise in improving lipid profile and hemodynamic picture in cardiovascular diseases.

Neuroprotective effect of Costus afer on low dose heavy metal mixture (lead, cadmium and mercury) induced neurotoxicity via antioxidant, anti-inflammatory activities.

Humans are constantly exposed to heavy metals due to their ubiquity in the environment. Hence, this study investigated the possible protective effect of Costus afer aqueous leaf extract (CALE) against low dose heavy metal mixture (LDHMM)-induced neurotoxicity. Male albino rats were divided into 6 equal groups. Group 1 served as the normal control receiving only deionized water. Group 2 served as the toxic control receiving on metal mixture (20 mg/kg PbCl2, 1.61 mg/kg CdCl2 and 0.40 mg/kg HgCl2), groups 3, 4 and 5 were co-treated with metal mixture and CALE (750, 1500 and 2250 mg/kg body weight, respectively) and group 6 was treated with metal mixture and ZnCl2. All treatments were administered through oral gavage for 90days. Oxidative stress biomarkers [malondialdehyde (MDA), superoxide dismutase (SOD), glutathione content (GSH) and catalase (CAT)], inflammatory cytokines [interlukin-6 (IL-6) and interlukin-10 (IL-10)], histopathological changes and heavy metal concentration were determined in brain of rats. Results indicated that LDHMM significantly increased (p < 0.05) the lipid peroxidation marker (MDA) and the pro-inflammatory cytokine (IL-6), while lowered levels of the oxidative biomarkers (SOD, CAT and GSH) and anti-inflammatory cytokine (IL-10). Also, LDHMM caused some histopathological changes such as reactive gliosis and glia cell proliferation. LDHMM elevated the lead, cadmium and mercury concentrations in the brain. Severity of the distorted cortical parameters were ameliorated by CALE administration. The CALE induced significant protective effect on LDHMM-mediated neurotoxicity in a dose-dependent manner which may be a result of its antioxidant anti-inflammatory and metal chelation mechanisms.

Low-dose heavy metal mixture (lead, cadmium and mercury)-induced testicular injury and protective effect of zinc and Costus afer in wistar albino rats.

The study evaluated the protective effect of Costus afer on low-dose heavy metal mixture (LDHMM)-mediated effects in the testis of albino rats. The weight-matched animals were divided into six groups: normal control, metal mixture of (PbCl2  + CdCl2 + HgCl2 ), combination of metal mixture + Costus afer at 750 mg/kg, combination of metal mixture + Costus afer at 1,500 mg/kg, combination of metal mixture + Costus afer at 2,250 mg/kg and combination of metal mixture + (ZnCl2 ). LDHMM reduced (p < .05) the antioxidant biomarkers (superoxide dismutase, SOD; catalase, CAT; and glutathione, GSH) and increased (p < .05) the lipid peroxidation marker (malondialdehyde, MDA) and lead, cadmium and mercury concentrations in the testis. Treatment with LDHMM increased (p < .05) abnormal sperm morphology and plasma prolactin (PRL) level and decreased epididymal sperm count, viability, follicle-stimulating hormone (FSH), luteinising hormone (LH) and testosterone. LDHMM exposure caused deleterious changes in the testis. Treatment of rats with Costus afer (750, 1,500 and 2,250 mg/kg) dose-dependently reduced (p < .05) the LDHMM-mediated toxicity. Treatment with Costus afer also reversed the testicular weight and LDHMM decrease in antioxidant biomarkers. Costus afer may be a defensive modulator of LDHMM-mediated testicular lesions.

Anicteric hepatoxicity: a potential health risk of occupational exposures in Nigerian petroleum oil refining and distribution industry.

BACKGROUND: Literature abounds linking one's job to certain unpalatable health outcomes. Since exposures to hazardous conditions in industrial environments often results in sundry health effects among workers, we embarked on this study to investigate the hepatic health effects of occupational activities in the petroleum refining and distribution industry. METHOD: Biochemical markers of liver functions were assayed in plasma, using Reflotron dry chemistry spectrophotometric system. The study was conducted on randomly selected workers of Port Harcourt Refining Company (PHRC) and Pipelines and Petroleum Product Marketing Company (PPMC) both in Alesa-Eleme near Port Harcourt, Nigeria, as well as non-oil work civil servants serving as control subjects. RESULT AND CONCLUSION: Results showed that, bilirubin ranged 0.3-1.6 mg/dl with a mean of 0.66±0.20mg/dl among the oil workers as against 0.5-1.00mg/dl with a mean of 0.58±0.13mg/dl in non-oil workers, Alkaline phosphatase ranged 50.00-296.00u/l (mean: 126.21±39.49u/l) in oil workers as against 40.20-111u/l (mean: 66.83±18.54u/l) for non-oil workers, Aspartic transaminases (AST) ranged 5.80-140.20u/l (mean: 21.81±11.49u/l) in oil workers against 18.00-44.00u/l (mean: 26.89±6.99u/l) for non-oil workers, while Alanine transaminases (ALT) ranged 4.90-86.00u/l (mean: 22.14±11.28u/l) in oil workers as against 10.00-86.60u/l (mean: 22.30±10.22u/l) for the non-oil workers. A close study of the results revealed that although the mean values for all the studied parameters were still within the parametric reference ranges, however, relative to the referents, there were significant increases (P<0.05) in plasma bilirubin (though anicteric) and alkaline phosphatase that was not matched with a corresponding increase in the plasma transaminases, suggesting a possibility that toxic anicteric hepatoxicity is part of the potential health effects of sundry exposures in the Nigeria petroleum oil refining and distribution industry. Gender differentiation data showed that though the mean values for the parameters were higher in males than females, the increases were not significant in most cases (P>0.05), whereas data for age and exposure period classifications revealed that irrespective of the age of the worker, the effects are likely to start after the first five years, manifesting fully after the first decade of occupational exposures. Thus, an update of industrial/occupational health measures is necessary for a safer and healthier work environment.