Downregulation of inflammatory erectile dysfunction by Mantisa religiosa egg-cake through NO-cGMP-PKG dependent NF-kB signaling cascade activated by mixture of salt intake.

We hypothesized whether 10% praying-mantis-egg-cake (10% PMEC) can be applied against inflammatory-erectile-dysfunction and whether it could be linked to NO-cGMP-dependent PKG signaling cascade. Ninety male albino-rats were randomly distributed into nine (n = 10) groups. Group I was given distilled water. Group II and III were pre-treated with 80 mg/kg NaCl and 75 mg/kg MSG, respectively. Group IV was pre-treated with 80 mg/kg NaCl + 75 mg/kg MSG. Group V was administered with 80 mg/kg NaCl+ 3 mg/kg Amylopidin. Group VI was given 80 mg/kg NaCl + 10% PMEC. Group VII was treated with 75 mg/kg MSG + 10% PMEC. Group VIII was treated with 80 mg/kg NaCl+ 75 mg/kg MSG + 10% PMEC. Group IX was post-treated with 10% PMEC for 14 days. Penile PDE-51, arginase, ATP hydrolytic, cholinergic, dopaminergic (MAO-A) and adenosinergic (ADA) enzymes were hyperactive on intoxication with NaCl and MSG. The erectile dysfunction caused by inflammation was linked to alteration of NO-cGMP-dependent PKG signaling cascade via up-regulation of key cytokines and chemokine (MCP-1). These lesions were prohibited by protein-rich-cake (10% PMEC). Thus, protein-rich-cake (10% PMEC) by a factor of 4 (25%) inhibited penile cytokines/MCP-1 on exposure to mixture of salt-intake through NO-cGMP-PKG dependent-NF-KB signaling cascade in rats.

Disorders of Hippocampus Facilitated by Hypertension in Purine Metabolism Deficiency is Repressed by Naringin, a Bi-flavonoid in a Rat Model via NOS/cAMP/PKA and DARPP-32, BDNF/TrkB Pathways.

Individuals who are hypertensive have a higher tendency of predisposition to other genetic diseases including purine metabolism deficiency. Therefore, the search for nontoxic and effective chemo protective agents to abrogate hypertension-mediated genetic disease is vital. This study therefore investigated the repressive effect of naringin (NAR) against disorder of hippocampus facilitated by hypertension in purine metabolism deficiency. Male albino rats randomly assigned into nine groups (n = 7) were treated for 35 days. Group I: control animals, Group II was treated with 100 mg/kg KBrO3, Group III was treated with 250 mg/kg caffeine, and Group IV was treated with 100 mg/kg KBrO3 + 250 mg/kg caffeine. Group V was administered with 100 mg/kg KBrO3 + 100 mg/kg haloperidol. Group VI was administered with 100 mg/kg KBrO3 + 50 mg/kg NAR. Group VII was administered with 250 mg/kg caffeine + 50 mg/kg NAR, and Group VIII was administered with 100 mg/kg KBrO3 + 250 mg/kg caffeine + 50 mg/kg NAR. Finally, group IX was treated with 50 mg/kg NAR. The sub-acute exposure to KBrO3 and CAF induced hypertension and mediated impairment in the hippocampus cells. This was apparent by the increase in PDE-51, arginase, and enzymes of ATP hydrolysis (ATPase and AMPase) with a simultaneous increase in cholinergic (AChE and BuChE) and adenosinergic (ADA) enzymes. The hypertensive-mediated hippocampal impairment was associated to alteration of NO and AC signaling coupled with lower expression of brain-derived neurotrophic factor and its receptor (BDNF-TrkB), down regulation of Bcl11b and DARPP-32 which are neurodevelopmental proteins, and hypoxanthine accumulation. However, these features of CAF-mediated hippocampal damage in KBrO3-induced hypertensive rats were repressed by post-treatment with NAR via production of neuro-inflammatory mediators, attenuation of biochemical alterations, stabilizing neurotransmitter enzymes, regulating NOS/cAMP/PKA and DARPP-32, BDNF/TrkB signaling, and restoring hippocampal tissues.

Meta-inhibition of ocular and gastrointestinal dysfunctions by phenolic-rich fraction of Croton zambsicus leaves in a rat model exposed to chronic mixed metals.

PURPOSE: This study was aimed at investigating the protective effect of antioxidant-rich fraction of Croton zambsicus (C-ZAMB) leaves on ocular-gastrointestinal dysfunction in rats exposed to environmental mixed-metal (EOMABRSL). MATERIALS AND METHODS: The rats were divided into five (n = 10) groups. Group I designates the control which received 0.5 mL of distilled water. Group II and III received 0.5 mL of EOMABRSL for 98 days (non-withdrawal) and 70 days (withdrawal for 28 days), respectively. Group IV received 0.5 mL EOMABRSL for 70 days and 400 mg/kg C-ZAMB fraction for 28 days. Group V received 400 mg/kg C-ZAMB only for 28 days via oral route. RESULTS: Exposure of the animals to EOMARBSL for 98 days and 70 days significantly up-regulated the activities of ocular-gastrointestinal aldolase-reductase, α-amylase, α-glucosidase and eco-51-nucleotidase with corresponding depletion of lactate dehydrogenase activity. Furthermore, exposure to EOMABRSL significantly altered the antioxidant proteins with up-production of MDA content. Apparently, management with 400 mg/kg C-ZAMB fraction significantly inhibited the key markers linked with ocular-gastrointestinal disorders. CONCLUSION: Hence, this study underscores the biochemical mechanisms for managing ocular-gastrointestinal lesions by 400 mg/kg C-ZAMB fraction on exposure to mixture of environmental metals.

Fansidar drug induces cytotoxicity in some vital tissues in a rat model: combination defensive effect of selenium and zinc capsules.

AIM: Fansidar (FAN) is widely used as an antimalarial drug, but it may cause hepatoxicity, nephrotoxicity, and neurotoxicity. Hence, the study examines the cytoprotection of selenium (Se) and zinc (Zn) tablets against FAN induced toxicity. METHOD: Group I was given distilled water. Groups II, III, IV, and V received 50 mg/kg FAN by gavage. Group III was co-treated with a 50 mg/kg Se tablet. Group IV was co-treated with a 50 mg/kg Zn tablet. Group V was co-treated with a 50 mg/kg Se tablet + 50 mg/kg Zn tablet. The exposure lasted for 7 days (sub-acute exposure). RESULT: FAN causes cytotoxicity through significant (p < 0.05) alteration of antioxidant molecules and hepatic enzymes. It also significantly (p < 0.05) induces renal, hepatocyte, and purkinje cell damage, but no visible lesion on testicular cells. The FAN induced cytotoxicity was significantly (p < 0.05) reversed on treatment with both single and combined antioxidant tablets. CONCLUSION: Our study supports the view that antioxidant micronutrient (Se and Zn) tablets may be a useful modulator in alleviating FAN induced oxidative stress and cytotoxicity in male rats. PLAIN LANGUAGE SUMMARY: Combined selenium and zinc capsules: better therapy against cytotoxicity Fansidar was approved by United States' Food and Drug Administration as an anti-malarial drug to treat acute and complicated malaria fever among patients in West Africa; however, its usage elicits toxicity to several organs of the body. It was elucidated that the combination of selenium and zinc capsules promotes organ wellness on co-treatment with Fansidar.

Metabolic depletion of synaptosomal enzymes linked with neurotoxicity and ovarian dysfunction by phenolic antioxidants of Croton zambsicus leaves in rats exposed to chronic mixture of anthropogenic toxicant.

A complex mixture of organic contaminants and metals is associated with neuron-fertility disorders and studies have demonstrated that phenolic antioxidants from herbal origin, possesses a strong protective potential. This study aimed to investigate the protection of phenolic croton zambesicus (C-ZAMB) leaves against neuro-ovarian damage in rats exposed to chronic mixture of anthropogenic toxicants (EOMABRSL). The animals were divided into five groups (n = 10): Group I was given 0.5 ml of distilled water only; Group II received 0.5 ml of EOMABRSL for 98 days; Group III received 0.5 ml of EOMABRSL for 70 days and withdrew for 28 days; Group IV received 0.5 ml of EOMABRSL for 70 days +400 mg/kg phenolic C-ZAMB for 28 days; Group V received 400 mg/kg C-ZAMB only for 28 days via oral route. Both non-withdrawal and withdrawal EOMABRSL-exposed animals exhibited neuro-ovarian impairment by up-regulating neuronal 51 eco-nucleotidase (51ENT), acetylcholinesterase (AChE), butrylcholinesterase (BuChE), synaptosomal monoamine oxidase-A (MAO-A) with altered cerebral antioxidants. Similarly, exposure to EOMABRSL for 98 and 70 days caused ovarian injury by amplifying the activity of 51ENT with corresponding decline of fertility index, lactate dehydrogenase (LDH) and Δ5 17ß-hydroxyl steroid dehydrogenase (Δ517ß-HSD). EOMABRSL intoxication also increased the neuro-ovarian MDA content with reduced numbers of neonates. Phenolic antioxidants from C-ZAMB leaves identified by High Pressure Liquid Chromatography (HPLC) ameliorated the chronic EOMABRSL intoxication. The treatment also prevented ovarian lesions by depleting MDA content and improved antioxidant status. Thus, confirming its neuro-ovarian protection.

Biogenic zinc-oxide nanoparticles of Moringa oleifera leaves abrogates rotenone induced neuroendocrine toxicity by regulation of oxidative stress and acetylcholinesterase activity.

Zinc oxide nanoparticles (ZnONPs) from plant origin were postulated to regulate complex hormonal control through the hypothalamus- pituitary-testicular axis and somatic cells due to their unique small size and effective drug delivery to target tissues. This study therefore investigates the biogenic synthesis of zinc oxide nanoparticles (ZnO NPs) from Moringa oleifera leaves on key endocrine hormones (LH, FSH and testosterone), MDA level, antioxidant enzymes (SOD and CAT), acetylcholineesterase (AChE) activity and reactive nitrogen species (NO•) level in rotenone induced male rat. The animals were divided into six groups (n = 8). Group I was orally given olive oil as vehicle; Group II received 60 mg/kg of rotenone (RTNE) only; Group III (RTNE + ZnONPs) received 60 mg/kg RTNE + 10 mg/kg ZnONPs; Group IV (RTNE + ZnCAP) received 60 mg/kg RTNE + 50 mg/kg zinc capsule; Group V (ZnONPs only) received 10 mg/kg ZnONPs only. Group VI received 50 mg/kg ZnCAP only. The experiment lasted 10 days. TEM and XRD images revealed ZnO NPs. Moreover, the presence of organic molecules in bio-reduction reactions from the FTIR spectrum showed the stabilization of the nanoparticles. Also, animals induced with rotenone exhibited impairment in the leydig cells by depleting LH, FSH, and testosterone levels with reduced AChE activity and significant (p < 0.05) alteration in cerebral enzymatic antioxidants. There was also brain increase in NO• production: marker of pro-inflammation. Nanotherapeutically, ZnONPs regulated hypothalamus-pituitary-testicular axis via modulation of cerebral NO•, FSH, LH, testosterone and AChE activity with induction of anti-oxidative enzymes.

Egg case concentrate of Mantis religiosa abrogates the accumulation of cadmium in muscular and bone tissues of African catfish via activation of nitric oxide and myeloperoxidase activity.

The study examined the prophylactic effect of praying mantis egg case powder (PMECP) against the accumulation of cadmium (Cd) in key tissues of African catfish (Clarias gariepinus). Thirty African catfish were randomly distributed into six (n = 5) groups. Group I was treated with normal fish diet (NFD) only. Group II was exposed to Cd + NFD. Group III was exposed to Cd + NFD + EC50 PMECP. Group IV was exposed to Cd + NFD + EC50 PMECP + 10% EC50 PMECP. Group V was exposed to Cd + NFD + EC50 PMECP + 20% EC50 PMECP. Group VI was treated with EC50 PMECP + NFD for 14 days. Inhibitory concentration (IC50 ) of PMECP significantly scavenged free radicals in vitro with corresponding increase in the activity of myeloperoxidase (MPO) and nitric oxide (NO) level. PMECP also showed highest growth-rate pattern and downregulation of cavitation within the lamellae. Hence, PMECP may be a prophylactic agent against the Cd accumulation in African catfish. PRACTICAL APPLICATIONS: Mantis religiosa egg case is widely used in Asian traditional medicine and some part of West Africa, as prevention against several diseases such as urinary disorders, infertility, impotence, and shingles. Our previous investigation showed that Mantis religiosa egg case flour could prevent hepatotoxicity, inhibit respiratory dysfunction, and interrupt oxidative damage in lungs. It is also commonly utilized for its high protein content and clear airways potential. The results of this study revealed empirical evidence concerning the possible usage of PMECP as natural, alternative, and/or complementary protein supplement with prophylactic potentials. Hence, this study underlines PMECP as prophylactic agent in abrogating the accumulation of cadmium as well as improving the protein content in African catfish.

Modulation of Cardiopulmonary Toxicity and Oxidative Stress by Phenolic-Rich Fraction of Croton zambiscus Leaves in Rat Exposed to Chronic Mixture of Environmental Toxicants.

Chronic mixed toxicant exposure has been implicated in the aetiology of lung and heart failure through prolonged free radical generations. This study was carried out to assess the protective effect of naturally occurring phenolic components from Croton zambesicus (400 mg/kg C-ZAMB) leaves against cardiopulmonary toxicity induced by chronic mixed toxicant (0.5 mL EOMABRSL) in rats. Chronic cardiopulmonary injury via oral administration of 0.5 ml EOMABRSL for 98 days (non-withdrawal) and 70 days (withdrawal) caused unhealthy alteration in the levels of oxidative stress biomarkers [malondialdehyde (MDA), reduced glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase]. Similarly, both withdrawal and non-withdrawal approaches of EOMABRSL-exposed animals exhibited increase in the activity of eco-51-nucleotidase (51ENT) with corresponding diminution in the activity of lactate dehydrogenase (LDH), i.e. the metabolic fuel for cardiopulmonary wellness. Ultimately, histology examination confirmed hyperplastic, bronchopneumonia and cloudy swelling of cardiovascular cells followed by the accumulation of cellular exudates and haemorrhage in the alveoli and bronchioles. The active antioxidants of 400 mg/kg C-ZAMB leaves were responsible for the biological protection of cardiopulmonary toxicity by modulating the activities of 51ENT and LDH. The oxidative stress was also reversed by 400 mg/kg phenolic C-ZAMB leaves in the heart and lungs. Hence, 400 mg/kg phenolic C-ZAMB leaves may be a natural therapy for the treatment of cardiovascular disorder associated with pulmonary dysfunction in rats.

Naringin attenuates Bisphenol-A mediated neurotoxicity in hypertensive rats by abrogation of cerebral nucleotide depletion, oxidative damage and neuroinflammation.

We examined whether active fruit naringin can reduce the risk of BPA-mediated neurotoxicity in L-NAME induced hypertensive rats and whether the modulation could be linked to improvement of brain NO signaling. Male albino rats were randomly distributed into eight (n = 7) groups. Group I was control animals, Group II was orally-treated with L-NAME, Group III was orally treated with 100 mg/kg BPA, Group IV was orally-treated with L-NAME +100 mg/kg BPA. Group V was orally-administered with L-NAME +80 mg/kg NAR. Group VI was orally-administered with 100 mg/kg BPA +80 mg/kg NAR. Group VII was orally-administered with L-NAME+100 mg/kg BPA +80 mg/kg NAR. Lastly, group VIII was orally-treated with 80 mg/kg NAR. The treatment lasted for 14 days. Sub-acute exposure to L-NAME and BPA induced hypertension and mediated-neuroinflammation at CA-2 and CA-4 of hippocampus cells. It was evident by increase in PDE-51 and enzymes of ATP hydrolysis (ATPase, ADPase and AMPase) with corresponding upsurge in cholinergic (AChE and BuChE), dopaminergic (MAO-A) and adenosinergic (ADA) enzymes as well as movement disorder. The hypertensive-mediated neurotoxicity was related to alteration of NO signaling and higher release of pro-inflammatory cytokines (TNF-α and IL-1ß), apoptotic proteins (P53 and caspace-9) and facilitated entry of T-lymphocytes (CD43+) into CNS through blood brain barrier potentiated by antigen presenting cells. Hence, these features of BPA-mediated neurotoxicity in L-NAME induced hypertensive rats were prohibited by co-administration of NAR through production of neuro-inflammatory mediators, stabilizing neurotransmitter enzymes, normalizing NO signaling and improving brain histology.

Naringin regulates erectile dysfunction by abolition of apoptosis and inflammation through NOS/cGMP/PKG signalling pathway on exposure to Bisphenol-A in hypertensive rat model.

This study investigated the effect of naringin (NRG) on extracellular metabolism of ATP through the NOS/cGMP/PKG signaling pathway induced by Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) on exposure to Bisphenol-A (BPA) in penis. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with 40 mg/kg L-NAME, Group III was treated with 50 mg/kg BPA, Group IV was treated with 40 mg/kg L-NAME +50 mg/kg BPA. Group V was administered with 40 mg/kg L-NAME +80 mg/kg NRG. Group VI was administered with 50 mg/kg BPA + 80 mg/kg NRG. Group VII was administered with 40 mg/kg L-NAME+50 mg/kg BPA + 80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG for 14 days. NRG prevented hypertension and erectile dysfunction by inhibiting the activities of angiotensin-converting enzymes, arginase, and phosphodiesterase-51 (PDE-51) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Additionally, hypertensive erectile dysfunction was remarkably prevented by NRG as manifested by the declined activities of AChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase and ADA) with resultant increase in NO level. Also, penile expression of antigen presenting cells, CD43 transcript, caspace-9 and tumor suppressor P53 proteins were repressed on treatment with NRG. This study validates the hypothesis that NRG may be a valuable remedy in abrogating penile inflammatory markers, apoptosis and enzymes of ATP-hydrolysis via NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to environmental toxicant.

Naringin protects against Bisphenol-A induced oculopathy as implication of cataract in hypertensive rat model.

People who have experienced high blood pressure are at greater risk of susceptibility to other health problems including oculopathy. The patients with these experiences do not have adequate treatment and those who do; spend much funds on the drug purchase. The study examines the protective effect of naringin (NRG) against ocular impairment in L-NAME induced hypertensive rat on exposure to a cellular disruptor. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), Group III was treated with 50 mg/kg Bisphenol-A, Group IV was treated with L-NAME +50 mg/kg Bisphenol-A. Group V was administered with L-NAME +80 mg/kg NRG. Group VI was administered with 50 Mg/kg BPA + 80 mg/kg NRG. Group VII was administered with L-NAME+50 mg/kg Bisphenol-A +80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG alone for 14 days. Naringin prevented hypertension and ocular dysfunction by depleting the activities of angiotensin-converting enzymes, arginase, aldose-reductase and phosphodiesterase-51 (PDE-51) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Moreover, ocular impairment was remarkably reduced by NRG as manifested by the decreased activities of AChE, BuChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase) and adenosine deaminase with resultant increased NO level. Also, ocular expression of CD43 transcript, caspaace-9 and tumor suppressor P53 proteins were suppressed on treatment with NRG. This study corroborates the view that NRG may be a useful therapy in alleviating inflammatory markers, apoptosis and metabolic nucleotides disorders via the NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to a cellular disruptor.

Rat liver and kidney post-mitochondrial dysfunction by addition of chronic mixed metal intoxication and hepatorenal wellness mediated by phenolic components from Croton zambiscus leaves.

Chronic exposure of mixed-metal intoxication has been associated with prolonged oxidative stress and severe hepatorenal damage. This present study demonstrates the hepatoprotective and renoprotective activity of Croton zambesicus (C-ZAMB) leaves, naturally occurring phenolic compounds against chronic mixed-metal (EOMABRSL) induced toxicity. 0.5 ml of EOMABRSL via oral route induced chronic hepatoxicity and nephrotoxicity on exposure for 98 days (non-withdrawal) and 70 days (withdrawal) by abnormal alteration in the levels of endogenous antioxidants. Moreover, EOMABRSL induced hepatorenal damage by increasing the markers of liver toxicity (ALT, AST, ALP, GGT and bilirubin) and kidney failure (creatinine, urea, uric acid, and renal electrolytes-Na+ and K+). Both non-withdrawal and withdrawal approaches of EOMABRSL-exposed animals exhibited hepatorenal dysfunctions by increasing the activity of eco-51-nucleotidase (51ENT) followed by the decreased in the activity of lactate dehydrogenase (LDH)-index of cellular ATP. These results were further supported by the histopathological examination of nephritic cells, hepatocytes and splenocytes, manifested by hepatocellular necrosis, swelling or degeneration of tubular kidney epithelial cells as well as coalescing splenic periarteriolar lymphoid sheaths (PALSs) and lymphoid haemosiderin. The chronic EOMABRSL intoxication was ameliorated by administration of phenolic antioxidants from C-ZAMB leaves. Therefore, our study supports the view that phenolic C-ZAMB leaves may mediate hepatorenal wellness on chronic exposure to mixed-metal intoxication.

Metabolic treatment of syndrome linked with Parkinson's disease and hypothalamus pituitary gonadal hormones by turmeric curcumin in Bisphenol-A induced neuro-testicular dysfunction of wistar rat.

The metabolic shift in cholinesterase activity and inhibitor of hypothalamus pituitary gonadal hormones were hypothesized as resultant effect of Parkinson's disease (PD) which is clinically characterized by a movement disorder. This study therefore examined the effect of turmeric curcumin (CUR) on index of PD, acetylcholine esterase activity and disorder of hypothalamus pituitary gonadal hormone (HPGH) in Bisphenol-A induced injury using animal model. Forty adult male albino rats were randomly distributed into five (n = 8) groups. Group I: vehicle control (olive oil 0.5 ml), Group II was given 50 mg/kg of BPA only, Group III was given 50 mg/kg BPA + 50 mg/kg curcumin, Group IV was given 50 mg/kg BPA + 100 mg/kg curcumin and Group V was administered 50 mg/kg of curcumin only for 14 days. The study examined the effect of curcumin on acetylcholineesterase (AChE) activity, nitric oxide radical (NO•) production, HPGH (LH, FSH and testosterone), MDA level, antioxidant enzymes (SOD and CAT), in BPA induced male rat. Sperm parameters were similarly examined. The animals induced with BPA exhibited impairment to striatum, leydig cells and sertoli cells by depleting LH, FSH, testosterone and spermatozoa with reduced AChE activity and significant (p < 0.05) alteration in cerebral enzymatic antioxidants. Locomotive activity was impeded followed by the increase of brain NO• level (marker of pro-inflammation). Therapeutically, CUR promoted hypothalamus-pituitary-testicular hormones via modulation of AChE and locomotive activities, reduction of intracellular NO• level, prevention of striatum-endocrine injury as well as oxidative damage. Hence, CUR abolished HPGH dysfunction linked with PD mediated by BPA in rat.

Toxicokinetics and Biliary Excretion of N-Nitrosodiethylamine in Rat Supplemented with Low and High Dietary Proteins.

Although biliary excretion is one of the biological elimination processes for foreign compounds, intake of high-protein diets was hypothesized to enhance their detoxification rates. Hence, this study investigates the effect of differential dietary protein intake on toxicokinetics and biliary excretion in rats following exposure to N-nitrosodiethylamine (NDEA) and aflatoxin B1 (AFB1). The animals were divided into five groups. Groups I and II were exposed to low and high dietary proteins following a single intraperitoneal dose of 43 µg NDEA/kg body weight, respectively. Groups III and IV were equally treated after a combined single intraperitoneal dose of 43 µg NDEA plus 0.022µg AFBI/kg body weight, respectively. Group V was fed with low-protein diets following a single intraperitoneal dose of 0.022µg AFB1/kg body weight. The experiment lasted 35 days. The bile excreted higher amounts of unchanged NDEA than nitrite. The groups placed on high-protein diets (HPD = 64%) eliminated higher amounts of the unchanged NDEA and nitrite than the lower-protein diet (LPD = 8%) groups. Furthermore, the animals fed with high dietary protein (HPD = 64%) depicted short half-life with corresponding increase in elimination rate constant. The presence of AFB1 heightened the excretion of bound NDEA with AFB1 than NDEA only. Generally, this study advocates that N-nitrosodiethylamine and the corresponding metabolites follow hepatobiliary system potentiated by high intake of dietary proteins.

Subchronic exposure to leachate activates key markers linked with neurological disorder in Wistar male rat.

The linking of various environmental chemicals exposure to neurodegenerative disorders is current. This study was undertaken to elucidate the toxic effects and the underlying biochemical mechanism of leachate obtained from Elewi Odo municipal battery recycling site (EOMABRL) using key markers of neuronal damage in rat via an oral route. Analysis of the concentrations of heavy metals showed that lead, cadmium, nickel, chromium, manganese, and iron were higher than the acceptable limits set by the regulatory authority-the World Health Organization. Whereas, copper, zinc, and cobalt were lower than permissible limits. EOMABRL was administered at 0, 20, 40, 60, 80, and 100% concentrations to adult male rats for 60 days. An in vitro study was also carried out in the cerebellum to assess cholinesterase biochemistry assays. Following exposure, brain was collected to determine the antioxidant status. EOMABRL administration significantly increased superoxide dismutase (SOD) and catalase (CAT) activities, and a sequential decrease in reduced glutathione (GSH) level with a concomitant increase in the accumulation of hydrogen peroxide (H2O2) and malondialdehyde (MDA) level was observed, when compared with the control. The treated rat had a significant (P < 0.05) increase in the activities of acetycholinesterase (AChE) and butyrylcholinesterase (BuChE). Taken together, these findings conclude that some possible mechanisms by which EOMABRL elicits neuronal disorder in male rat could be through the activation of AChE and BuChE and induction of oxidative stress with necrosis of neuronal cells.

Depletion of cellular adenosine triphosphate and hepatocellular damage in rat after subchronic exposure to leachate from anthropogenic recycling site.

One of the major hazards arising from recycling sites is the generation of leachate containing mixed metal. This study evaluated the toxic effects of leachate obtained from Elewi Odo municipal auto-battery recycling site (EOMABRSL) on male liver functions using hepatic indices and biomarker of cellular adenosine triphosphate (ATP) in rat via the oral route. Concentrations of heavy metals analysis showed that lead, cadmium, nickel, chromium, manganese, and iron were 1.5-, 2-, 2.5-, 1.36-, 19.61-, and 8.89-folds, respectively, higher than acceptable limits set by regulatory authority World Health Organization. Copper, zinc, and cobalt were 5.9-, 300-, and 1.02-folds, respectively, lower than permissible limits. The EOMABRSL was administered at 20, 40, 60, 80, and 100% concentrations to adult male rats for 60 days. Following exposure, plasma and livers were collected for several biochemistry assays. Exposure of animals to EOMABRSL resulted in 27.51, 28.14, 63.93, 28.42, and 40.16% increase in aspartate aminotransferase activity, whereas it elevated alanine aminotransferase activity by 5.35, 22.33, 88.68, 183.02, and 193.08%, respectively, when compared with the control. Similarly, γ-glutamyl transferase activity increased by 111.22, 114.19, 122.96, 573.14, and 437.02%, respectively, when compared with the control. EOMABRSL administration significantly decreased catalase activity and reduced glutathione level and superoxide dismutase with concomitant increase in malondialdehyde and hydrogen peroxide levels. Also, significant (p < 0.05) decrease in lactate dehydrogenase (LDH) activity (marker of cellular ATP) was observed. Taken together, the hepatotoxicity of EOMABRSL could be due to the depletion of LDH and induction of oxidative damage, which may suggest possible health hazards in subjects with occupational or environmental exposure.

Inhibition of key markers linked with spermatogenesis and cellular ATP by subchronic exposure to leachate in a rat model.

Few or no studies have measured the toxic effects of subchronic exposure to leachate using key markers linked with spermatogenesis and cellular adenosine triphosphate (ATP) in an experimental rat model. This study was undertaken to evaluate the toxic effects of leachate obtained from the Elewi Odo municipal battery-recycling site (EOMABRL) on male reproductive function using testicular hormones and biomarker of cellular ATP. EOMABRL was administered at 0, 20, 40, 60, 80, and 100% concentrations to adult male rats for 60 days. After exposure, serum was collected for hormonal biochemistry assays, and testes were collected to determine the activity of xanthine oxidase (XO) and lactate dehydrogenase (LDH). Exposure of animals to EOMABRL resulted in a 519.7, 285.7, 569.1, 606.1, and 1,793.2% increase in XO activity with a sequential decrease in LDH activity (marker of cellular ATP) by 44.1, 55.9, 61.4, 69.3, and 89.7%, respectively, compared with the control. Furthermore, EOMABRL caused a significant inhibitory effect on serum luteinizing hormone, follicle-stimulating hormone, and testosterone levels. We conclude that some possible mechanisms by which EOMABRL elicits toxicity in male rat testes could be through inhibition of LDH activity and depletion of serum hormone levels.

Municipal landfill leachate induces hepatotoxicity and oxidative stress in rats.

Human beings are more often exposed to complex mixtures of hazardous chemicals than single toxicant. The present study investigated the effects of Olushosun municipal landfill leachate (OMLL) from Ojota in Lagos State of Nigeria on hepatic function and some biomarkers of oxidative stress in adult rats. Physicochemical characteristic analysis of OMLL showed that while total alkalinity, total acidity, total hardness, biochemical oxygen demand and chemical oxygen demand were 3-fold, 2-fold, 4-fold and 1-fold, respectively, concentrations of heavy metals analysis showed that copper, lead, cadmium, arsenic, cobalt, chromium and mercury were 9-fold, 4-fold, 21-fold, 1320-fold, 7-fold, 5-fold and 4-fold, respectively, higher than acceptable limits by regulatory authorities. The OMLL was administered at 0, 10, 20, 30 and 40% concentrations to adult male rats for 14 days. Following exposure, serum was collected for serum biochemistry assays and liver was collected to determine the antioxidant status. Exposure of animals to 10, 20, 30 and 40% OMLL resulted in 3%, 31%, 52% and 83% increase in aspartate aminotransferase activity, whereas it elevated alanine aminotransferase activity by 10%, 25%, 30% and 49%, respectively, when compared with the control. While OMLL administration significantly increased catalase activity, a sequential decrease in reduced glutathione level and in superoxide dismutase and glutathione-S-transferase activities with concomitant increase in malondialdehyde level were observed, when compared with the control. Collectively, the hepatotoxicity of OMLL could be due to the induction of oxidative stress and may suggest possible health hazards in subjects with occupational or environmental exposure.