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Lead (Pb) is a ubiquitous, non-biodegradable heavy metal contaminant with a significant impact on both human and animal health. The adverse effect of lead on health and productivity of avian species has received little attention. Alchornea laxiflora (Benth) belongs to Euphorbiaceae family and grows naturally in the Nigerian rain forest. Decoction of the leaves is usually administered traditionally to treat inflammatory and infectious diseases. The ethanol extract of Alchornea laxiflora (EaAL) leaves was used in this study to ameliorate lead-induced neurodegeneration.Seven groups of 5-week-old cockerels (n=5) were treated for 6 weeks thus: Group A - Control (water only), Group B - (100 mg/kg of EaAL daily), Group C - (200 mg/kg of EaAL daily, p.o.), Group D - (1 % lead acetate in drinking water), Group E - (1 % lead acetate in drinking water and 100 mg/kg of EaAL daily), Group F - (1 % lead acetate and 200 mg/kg of EaAL daily), Group G - (1 % lead acetate and 100 mg/kg of Vitamin C). All administrations were per os birds were euthanized on day 43 by quick cervical dislocation. Histological stains (H&E and Nissl) and Black Gold II (BGII) histochemistry were used to assess alterations in the cerebrum and cerebellum.Administration of EaAL at the two concentrations resulted in a drastic reduction in the incidence of neuropathologies observed (e.g. pyknosis and multilayering of Purkinje cells, neuronal degeneration in hippocampus cerebrum and ependymal cells, distortion of meningeal epithelial cells, etc). BGII histochemistry revealed severe demyelination caused by the administration of lead acetate, while the two doses of EaAL showed significant restoration of myelin in the cerebellum. The amelioration of demyelination observed with the use of vitamin C was considerably lower than that recorded with the use of EaAL.The use of EaAL significantly ameliorated morphological alterations and demyelination caused by the administration of lead acetate, however, caution should be exercised in the administration, as individual species idiosyncrasies may arise and the tendency to pro-oxidation at 200 mg/kg when administered alone was observed in one subject.

Introduction: Alterations of antioxidant defense, neuroinflammation, and neurodegeneration are common pathological occurrences associated with neurodegenerative diseases. This study evaluated the neuroprotective effect of Launaea taraxacifolia (LT), popularly known as African Wild lettuce, against neuroinflammation, memory loss, and neurobehavioral deficit. Methods: Adult Wistar rats were used following random assignment into groups 1 to 5. Group one was the normal control. Groups four to five received 40 mg/kg Nω-nitro-l-arginine methyl ester (L-NAME). In addition to L-NAME exposure, groups three and four received 100 and 200 mg/kg LT, whereas group five received 10 mg/kg lisinopril. The experiment lasted for five weeks. Markers of oxidative stress, neurobehavioural studies, histology, and immunohistochemistry of glial fibrillary acidic protein (GFAP), ionised calcium-binding adaptor molecule 1 (Iba-1), as well as anti-calbindin for staining astrocytes, microglia, and Purkinje cells were determined. Results: Malondialdehyde (MDA) and protein carbonyl in the L-NAME alone group were heightened compared to those treated with LT. However, treatment with LT significantly reduced neuronal oxidative stress, neuroinflammation, and neurobehavioural changes. Quantitative analysis of immunohistochemical staining revealed heightened glial fibrillary acidic protein (GFAP), ionised calcium-binding adaptor molecule 1 (Iba-1), as well as anti-calbindin as indicated by astrogliosis, microgliosis, and Purkinje cell degeneration in untreated rats. Moreover, the observed ultrastructural anarchy induced by L-NAME was restored in rats treated with LT (P

Objective: Curcuma longa Rhizome (CLR), due to its potent antioxidant phytochemical constituents, was investigated for its effects on bisphenol A (BPA)-induced cardiovascular and renal damage.Materials and Methods: Sixty rats were randomly selected, and grouped as control, BPA (100 mg/ kg), BPA and CLR 100 mg/kg, BPA and CLR 200 mg/kg, CLR 100 mg/kg, and CLR 200 mg/kg for 21 days. Oxidative stress indices, antioxidant status, blood pressure parameters, genotoxicity, and immunohistochemistry were determined.Results: Rats exposed to the toxic effects of BPA had heightened blood pressure, lowered frequency of micronucleated polychromatic erythrocytes, and decreased activities of antioxidant enzymes compared with rats treated with CLR. Moreover, administration of CLR significantly (p

Objective: Lead (Pb) poisoning affects multiple organs including the reproductive system. The experiment was performed to explore the protective effect of naringin on testicular apoptosis, neuronal dysfunction and markers of stress in cockerel chicks.Materials and Methods: Thirty-six cockerel chicks were used for this study, and randomly grouped into six chicks per group viz. control, Pb only (600 ppm), Pb and naringin (80 mg/kg), Pb and Naringin (160 mg/kg), naringin only (80 mg/kg) and naringin only (160 mg/kg), respectively, for eight weeks. Pb was administered via drinking water while naringin was administered via oral gavage. Oxidative stress indices in the brain and testes were assessed, and immunohistochemistry of TNF-α and caspase 3 was done in the brain and testes, respectively.Results: Lead administration induced inflammatory and testicular apoptosis cascade accompanied with increased oxidative stress and upregulation of brain and testicular antioxidant enzymes in comparison to the control and Pb-only-treated cockerels. Immunohistochemistry showed significant immunoreactivity of testicular caspase 3 and TNF-α in the brain.Conclusion: Treatment of Pb-exposed chickens with naringin offered protection to Pb acetate-induced testicular oxidative stress, apoptosis, and neuroinflammation in cockerel chicks.

Abstract Background The important roles of liver and kidney in the elimination of injurious chemicals make them highly susceptible to the noxious activities of various toxicants including cobalt chloride (CoCl2). This study was designed to investigate the role of glycine in the mitigation of hepato‐renal toxicities associated with CoCl2 exposure. Methods Forty‐two (42) male rats were grouped as Control; (CoCl2; 300 ppm); CoCl2 + Glycine (50 mg/kg); CoCl2 + Glycine (100 mg/kg); Glycine (50 mg/kg); and Glycine (100 mg/kg). The markers of hepatic and renal damage, oxidative stress, the antioxidant defense system, histopathology, and immunohistochemical localization of neutrophil gelatinase associated lipocalin (NGAL) and renal podocin were evaluated. Results Glycine significantly reduced the markers of oxidative stress (malondialdehyde content and H2O2 generation), liver function tests (ALT, AST, and ALP), markers of renal function (creatinine and BUN), and decreased the expression of neutrophil gelatinase‐associated lipocalin (NGAL) and podocin compared with rats exposed to CoCl2 toxicity without glycine treatment. Histopathology lesions including patchy tubular epithelial necrosis, tubular epithelial degeneration and periglomerular inflammation in renal tissues, and severe portal hepatocellular necrosis, inflammation, and duct hyperplasia were observed in hepatic tissues of rats exposed to CoCl2 toxicity, but were mild to absent in glycine‐treated rats. Conclusion The results of this study clearly demonstrate protective effects of glycine against CoCl2‐induced tissue injuries and derangement of physiological activities of the hepatic and renal systems in rats. The protective effects are mediated via augmentation of total antioxidant capacity and upregulation of NGAL and podocin expression.

Introduction: Cisplatin (CP)-induced toxicity involves oxidative stress and Picralima nitida is rich in natural antioxidants hence its methanol leaf extract was used to mitigate the toxic effect of CP.Methods: Forty rats divided into four groups of 10 rats per group were used as follows: group A (normal saline), group B (CP 10 mg/kg), group C [Methanol Leaf Extract of Picralima nitida (MLEPN), 100 mg/kg and CP 10 mg/kg], and group D (MLEPN 200 mg/kg and CP 10 mg/kg). All administrations were done by oral gavage with the volumes of the treatments administered determined by the average weight of the rats in each group except CP, which was given intraperitoneally. Administration of normal saline and MLEPN lasted for seven consecutive days after which a single dose of CP was given on day 8. All animals were sacrificed 72 hours after CP administration. On day 9, blood pressure measurement was taken, and changes in body weight were determined. On day 10, blood samples were taken for serum chemistry, and kidneys, liver, and heart were harvested from the animals for Serum assay, histopathology, and immunohistochemistry, respectively.Results: The extract improved weight changes caused by CP and reversed the toxic changes produced by CP on serum chemistry, oxidative stress, and histopathology. The extract caused a significant decrease in the levels of nuclear factor kappa beta, cardiac troponin, and mineralocorticoid receptors (MCRs). However, it increased the protein expression of Nrf2 compared to the toxicant group.Conclusion: The extract exhibited anti-inflammatory, antioxidant, and anti-renin properties.

Abstract Dietary sources of functional foods and nutraceutical have shown strong potentials in the management of hypertension and its complications. Sandpaper leaves, Ficus asperifolia Miq (FA), particularly found in Africa has a rich folkloric history in the management of diabetes and hypertension. This study produced biscuits supplemented with blends of FA at 2.5% and 5% fed to Nw (G)‐nitro‐l‐arginine‐methyl‐ester (L‐NAME, 40 mg/kg/day) induced‐hypertensive rats for 14 days followed by the assessment of blood pressure, lipid profile, and atherogenic index in hypertensive rats. The phenolic constituents of FA blends were analyzed using high‐performance liquid chromatography diode‐anode (HPLC‐DAD). Thereafter, the mean arterial blood pressure (MABP) and systolic blood pressure (SBP) was measured using the tail‐cuff method after which the heart and lungs of rats were collected, weighed, and the antioxidant status and lipid cholesterol profile were assessed. We realized that recorded phenolic constituents in extracts of FA was at a high level and FA enriched biscuit‐diet caused a significant decrease in SBP and MABP in L‐NAME‐induced hypertensive rats, body weight, atherogenic index and cholesterol profile in treated rats. However, FA enriched biscuit resulted in increased activities of catalase (CAT), superoxide dismutase (SOD), and glutathione‐S‐transferase (GST) antioxidant enzymes in the heart and lungs of hypertensive rats. This study revealed that FA enriched biscuit‐diet does not only have antihypertensive and antioxidant potential in L‐NAME‐induced hypertensive rats but also plays a protective role in the management of hyperlipidemia.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of coronavirus disease 2019 (COVID-19). This virus has become a global pandemic with unprecedented mortality and morbidity along with attendant financial and economic crises. Furthermore, COVID-19 can easily be transmitted regardless of religion, race, sex, or status. Globally, high hospitalization rates of COVID-19 patients have been reported, and billions of dollars have been spent to contain the pandemic. Angiotensin-converting enzyme (ACE) 2 is a receptor of SARS-CoV-2, which has a significant role in the entry of the virus into the host cell. ACE2 is highly expressed in the type II alveolar cells of the lungs, upper esophagus, stratified epithelial cells, and other tissues in the body. The diminished expressions of ACE2 have been associated with hypertension, arteriosclerosis, heart failure, chronic kidney disease, and immune system dysregulation. Overall, the potential drug candidates that could serve as ACE2 activators or enhance the expression of ACE2 in a disease state, such as COVID-19, hold considerable promise in mitigating the COVID-19 pandemic. This study reviews the therapeutic potential and pharmacological benefits of the novel ACE2 in the management of COVID-19 using search engines, such as Google, Scopus, PubMed, and PubMed Central.

Objective: The ameliorative effect of Annona muricata in glycerol-induced acute kidney injury in laboratory rats was evaluated. Methods: Thirty albino rats were used and were divided into five of six rats per group. The first (control) group was given distilled water (2 ml/kg) for seven days, while the second (toxicant or glycerol alone) group was given only glycerol (10 ml/kg) on day 8. The third, fourth, and fifth groups received methanol leaf extract of Annona muricata (100 mg/kg), 200 mg/kg dose of the extract, and enalapril (10 mg/kg) respectively for seven days, and on day eight all received glycerol (10 ml/kg). Serum chemistry, histopathology, immunohistochemistry, and changes in blood pressure were indices of toxicity. Results: In the toxicant group, blood pressure increased significantly (p

Background and Aim: Momordica charantia is a highly valued plant, widely distributed in the tropical and subtropical regions. The plant is reported to have a wide range of medicinal uses. This study was designed to explore the ameliorative potential of M. charantia methanol leaf extract in alloxan-induced diabetic animal model with a particular focus on the liver. Materials and Methods: Hepatoprotective effect of methanol leaf extract of M. charantia was assessed in alloxan-induced toxicity in 50 rats divided into five groups (A-E) (n=10). Group A normal control, Group B was toxicant group, and Group C animals received glibenclamide treatment while Groups D and E received extracts at 200 and 400 mg/kg doses, respectively. The experiment lasted for 28 days. Histopathological changes, blood glucose level, and serum enzymes such as aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, oxidative status and caspase-9, and interleukin-1β (IL-1β) were evaluated. Results: Extract-treatment caused a decreased blood glucose level, markers of oxidative stress such as malondialdehyde and hydrogen peroxide (H2O2). Treatment of rats with leaf extract of M. charantia resulted in increased levels and activities of protein thiols, non-protein thiols, glutathione (GSH), glutathione peroxidase, glutathione S-transferase, and superoxide dismutase indicating its antioxidant potential. The liver section revealed mild distortion of the hepatic architecture compared to the toxicant group, while decreased expressions of caspase-9 and IL-1β in extract-treated groups was observed. Conclusion: The plant extract exhibited antioxidant, anti-apoptotic, and anti-inflammatory effects, thus showing its hepatoprotective property.

Background and Aim: High salt diet and uninephrectomy are associated with high blood pressure with attendant cardiovascular disease conditions such as hypertension, renal damage, myocardial infarction, and stroke. The aim of this study was to investigate the beneficial effects of consumption of cocoa and cocoa-containing products in the management of high blood pressure in uninephrectomized hypertensive rats. Materials and Methods: The effect of cocoa powder on blood pressure, markers of inflammation, oxidative stress, and histopathology were investigated in uninephrectomized animals fed with cocoa feed alone or in combination with a high salt diet. Male rats were randomly divided into five groups: Group A was the control group and fed with normal feed alone, Group B was fed with cocoa feed alone, Group C was fed with high salt diet (8% salt), Group D was fed with cocoa-feed compounded with 8% salt for 4 weeks after uninephrectomy, and Group E was uninephrectomized rats on a normal diet. The left kidneys of animals in Groups C, D, and E were removed by surgery. After 4 weeks of treatment, the systolic, diastolic, and mean arterial blood pressure was measured. The serum markers of renal damage and oxidative stress were determined. Histological examination was also performed on renal and cardiac tissues. Results: Results showed significant increases in biomarkers of oxidative stress, inflammation, and renal damage with a concomitant decrease in antioxidant status in hypertensive uninephrectomized rats. Cocoa feed, however, significantly improved blood pressure and nitric oxide bioavailability, antioxidant status and reduced markers of inflammation and oxidative stress. Conclusion: These findings show that cocoa powder could be used to maintain blood pressure levels in hypertensive rats through its antioxidant capacity.

The anti-diabetic property of aqueous leaf extract of Moringa oleifera was performed in streptozocin-induced diabetic rats using serum chemistry, histology and immunochemical parameters as indices of diabetes. The blood glucose level of the diabetic untreated group continues to increase while that of the treated group after 21 days decreased. While the animals in the diabetic untreated group experienced increase in the levels of markers of organ damage when compared to the control group (P values < 0.0001). ALT increased from 61.83±1.5 to 96.1±22.4, AST was 225.1±26.6 from 172.6±13.9, ALP 13.5±0.006 to 13.6±0.002, UREA 1.0±0.08 to 3.0±0.4, their reduction was observed in the extract-treated groups. ALT reduced from 96.1±22.4 to 73.70±9.7; AST from 225.1±26.6 to 184.4±18.2; ALP from 13.6±0.002 to 13.6±0.01; UREA from 3.0±0.4 to 2.0±0.4. Treatment with the extract significantly reduced markers of oxidative stress in the kidney [hydrogen peroxide (898.8±6.26 to 688.0±13.7), malondialdehyde (640±0.1 to 600±0.2) and protein carbonyl (548.4±1.5 to 458.1±1.6)]; heart [hydrogen peroxide (389.4±1.8 to 358.2±1.5), malondialdehyde (264.0±0.5 to 122.0±0.3), protein carbonyl (196.8±0.5 to 162.7±3.5)]; and liver [hydrogen peroxide (119.36±3.2 to 103.94±10.7), malondialdehyde (236.0±0.4 to 73.0±0.2), protein carbonyl (269.3±1.0 to 174.2±1.1) respectively. The levels of antioxidants were reduced in the diabetic untreated group but there was increase in the Moringa treated group. Glucose transporter 4 (GLUT 4) was down regulated in the diabetic untreated group while it was well expressed in the treated groups. The histology of pancreas and liver showed varied levels of infiltration of inflammatory cells, congestion and necrotic lesions, but these were mild in the treated groups. The result shows that the extract does have an anti-diabetic effect with the decrease in the levels of blood glucose and markers of oxidative stress as well as increase in the amount of antioxidants in the treated group when compared to the diabetic untreated group. More importantly, the extract caused upregulation of GLUT 4, which is relevant in reversing insulin resistance in the same manner as pioglitazone, the standard antidiabetic agent used in this study.

Moringa oleifera popularly referred to as wonder plant is a medicinal plant with a remarkable variety of therapeutic purposes. The aim of this study was to assess the ameliorative effect of Moringa oleifera on glycerol-induced acute kidney injury in rats thus renewing interest in the development of new treatment plans. Glycerol (50% v/v in sterile saline, intramuscular) was used to induce acute kidney injury. Group A (control group) received distilled water only, the group B animals (toxicant group) received glycerol alone on the 8th day, and groups C and D animals were given 50 mg/kg and 100 mg/kg of methanol stem extract of Moringa oleifera respectively for seven days and glycerol on the 8th day. Group E animals on the other hand received 100 mg/kg of methanol stem extract of Moringa oleifera alone for seven days and on day 8 received normal saline. To assess renal damage and possible ameliorative effects of the extract, serum blood urea nitrogen (BUN), creatinine, myeloperoxidase, advanced oxidative products, malondialdehyde, superoxide dismutase, reduced glutathione, and protein carbonyl were determined. Histopathological analysis of kidney tissues and immunohistochemical analysis of KIM-1 and NF-ҝB expressions were also carried out on kidney tissues. The results showed that methanol stem bark extract of Moringa oleifera improves glycerol-induced acute kidney injury by inhibiting markers of inflammation, oxidative stress and renal damage by modulating KIM-1 and NF-ҝB signaling pathways. In conclusion, the methanol stem extract of Moringa oleifera blunts glycerol-induced acute kidney injury in rats through its anti-oxidant and anti-inflammatory properties.

Arsenic acid is one of the abundant environmental pollutants present in soil, water and the air. Undoubtedly, it has found its way to the food chain in which humans and animals are the final targets thereby causing arrays of disease conditions including cardiovascular and renal dysfunction. Hence, the use of phytochemicals present in medicinal plants has gained global acceptance as chemotherapeutic agents that can prevent, ameliorate, reverse or treat diseases. From our study, arsenic acid intoxication led to significant increase in heart rate (HR), QRS, together with prolonged QT and QTc interval. However, Kolaviron (KV) at the dosage of 100 and 200 mg/kg body weight reversed the aforementioned electrocardiographic (ECG) changes. KV pre-treatment also ameliorated cardiorenal dysfunction via significant reduction in cardiac and renal markers of oxidative stress such as malondialdehyde, hydrogen peroxide generation, myeloperoxidase activity and nitric oxide contents. Immunohistochemistry revealed expressions of renal C-reactive proteins (CRP) and expressions of anti-apoptotic protein BCL2 in KV treated rats. Furthermore, cardiac troponin I (CTnI) expressions were lower in KV treated rats. Taken together, KV mitigated arsenic-acid induced cardiovascular dysfunction via up-regulation of antioxidant defense system and down-regulation of inflammatory and apoptotic signaling pathways. Keywords: Kolaviron, Arsenic acid, Oxidative stress, Cardiovascular dysfunction, Chemoprevention

Background: Parquetina nigrescens (Afzel.) Bullock of the family Asclepiadaceae is known for its antioxidant effects with wide range of uses in Southwestern Nigeria especially in traditional medicine. This study was undertaken to explore if polyphenol-rich fraction (prf) from P. nigrescens will ameliorate dichlorvos-induced neurotoxicity and apoptosis. The exploration utilized evaluation of markers of oxidative stress, apoptosis and serum acetylcholinesterase (AchE) levels. Methods: Forty Wistar rats randomly placed in four groups were utilized for the study. Animals in Group A received corn oil, group B- dichlorvos (16 mg/kg), groups C and D- dichlorvos + 100 and 200 mg/kg prf of P. nigrescens respectively. Markers of oxidative stress, antioxidants and apoptosis were assessed in the serum and brain tissues using biochemical assay and immunohistochemistry. Results: Exposure to dichlorvos caused significant decreases in AchE, catalase, superoxide dismutase, glutathione peroxidase (GPx) and increases in hydrogen peroxide (H2O2) generation and malondialdehyde levels. Histopathology and immunohistochemistry of the cerebellum and cerebrum of rats exposed to dichlorvos revealed greater neurotoxic effects in the cerebellum as well as decreased expressions of AchE with a concomitant increase in Bax (proapototic) compared to prf of P. nigrescens treated rats. Conclusion: This study showed that dichlorvos caused cellular and tissue neurotoxicity by inhibiting AchE activity, induced oxidative stress and apoptosis in rats with prominent effects on the cerebellum than cerebrum. The prf of P. nigrescens showed amelioration of neurotoxicity by its antioxidative and antiapoptotic properties in rats exposed to dichlorvos.

Background: Azadirachta indica is widely distributed in Africa, Asia and other tropical parts of the world. A. indica (AI) is traditionally used for the treatment of several conditions including cancer, hypertension, heart diseases and skin disorders. Intestinal ischaemia-reperfusion is a common pathway for many diseases and may lead to multiple organ dysfunction syndrome and death. Objective: In this study, we investigated the ameliorative effects of AI on intestinal ischaemia-reperfusion injury-induced cardiorenal dysfunction. Materials and methods: Sixty rats were divided into 6 groups; each containing 10. Corn oil was orally administered to group A (control) rats for 7 days without intestinal ischaemia-reperfusion injury. Group B underwent intestinal ischaemia-reperfusion injury (IIRI) without any pre-treatment. Groups C, D, E and F were pre-treated orally for 7 days with 100 mg/kg AI (100 and (200 mg/kg) vitamin C (100 and 200 mg/kg) respectively and thereafter underwent IIRI on the 8th day. Results: The cardiac and renal hydrogen peroxide increased significantly whereas serum xanthine oxidase and myeloperoxidase levels were significantly elevated (p

Purpose: Vernonia amygdalina is a medicinal plant of great importance that has its fresh leaves rich in vitamins and salt hence, it is valuable in human diet. The anti-oxidant, anti-inflammatory and analgesic activities of its acetone leaf extract were evaluated in this study to validate its folkloric use. Methods: The acetone extract is prepared by dissolving ground plant materials (200g) in 1 L of acetone for 48 h, filtered, and then dried using rotary evaporator before it is used for the pharmacological investigations. Standard phytochemical methods were used to test for the presence of phytoactive compounds in the plant. Acute toxicity was carried out in mice to determine safe doses for use. The anti-inflammatory activities were conducted using carrageenan and histamine to induce oedema in rats while analgesic activities were embarked upon using acetic acid- induced writhing test and formalin-induced paw lick test. The anti-oxidant activities were assessed in vitro using ABTS, DPPH, FRAP and total polyphenolics. Results: The results from this study showed that the 100 and 200 mg/kg doses of the acetone extract caused significant reduction in oedema induced by both carrageenan and histamine. Similar effect was observed in analgesic tests which were comparable to that of indomethacin, the reference drug used in the study. Conclusion: The anti-oxidant effects were also good and the pharmacological activities may be due to the presence of polyphenols and other phytochemicals contained in the plant. The study may have thus validated the folkloric use of this plant as a medicinal and nutritional agent.

Background: Gallic acid (GA) is an endogenous plant phenol known to have antioxidant, free radical scavenging ability, anti-inflammatory, anti-cancer, and anti-fungal properties. The aim of this study was to assess the protective effect of GA on cyclophosphamide (CPA)-induced hepatotoxicity in male Wistar rats. Methods: Sixty rats were grouped into six groups of 10 rats per group. Group 1 received distilled water. Group 2 received CPA at 200 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 received a single dose of CPA (200 mg/kg) intraperitoneally on day 1 and then were treated with GA at 60 and 120 mg/kg body weight for 14 days, respectively. Rats in Groups 5 and 6 only received GA at 60 and 120 mg/kg body weight for 14 days, respectively. GA was administered orally. Results: CPA induced hepatic damage as indicated by significant elevation (P < 0.05) in aspartate aminotransferase, organ weight, and evidence by the histological study. CPA also induced hepatic oxidative stress as indicated by significant elevation (P < 0.05) in malondialdehyde content, hydrogen peroxide (H 2 O 2 ) generation, nitrite level, and the level of glutathione (GSH) peroxidase crashed in the CPA-treated group. GA enhanced the antioxidant defense system as indicated by significant elevation (P < 0.05) in GSH level, catalase activity, and GSH-S-transferase activity. Conclusions: Taken together, the result of this present study shows that GA has a protective effect on CPA-induced hepatotoxicity.

Background: Oral ingestion of lead in drinking water represents the most common route of human and animal exposure, especially in the developing nations. Unlike other internal organs, research on the effects of lead on gastrointestinal tract remains limited. This study explored the alterations in faecal fatty acid composition, gastrointestinal and hepatic histologies and redox status, following chronic, 90-day exposure of rats to lead acetate (PbA). We also investigated the protective effects of rutin and melatonin against lead toxicity in rats. Methods: Fifty male Wistar rats were randomly divided into five groups of 10 (A-E) and were assigned as follows: A: Control; B: 1% PbA in drinking water; C: PbA+rutin (50 mg/kg); D: PbA+melatonin (25 mg/kg) and E: PbA+rutin+melatonin. The faecal fatty acid profiles were quantified by methylation and gas chromatography-flame ion detection. We also evaluated the oxidative stress and antioxidant markers for the stomach, liver, and guts, and their histopathological alterations. Results: Exposure to PbA caused remarkable elevations of the faecal fats, such as undecylic, lauric, tridecylic, myristic, and palmitic acids, compared to the controls and rats in group C. The administration of rutin and/or melatonin ameliorated the PbA-induced increases in the hydrogen peroxide and malondialdehyde contents. Rutin and melatonin improved the levels of thiol, and reduced the glutathione, glutathione S-transferase and superoxide dismutase activities. Conclusion: The findings suggest that rutin alone or combined with melatonin protects against PbA-induced disruption of the liver and gastrointestinal tract integrity via modulation of intestinal total lipids in cells and redox imbalances. [ABSTRACT FROM AUTHOR]