Protective mechanisms of 6-gingerol in dextran sulfate sodium-induced chronic ulcerative colitis in mice.

Ulcerative colitis (UC) is a relapsing and remitting inflammatory disease of the colon, with an increasing incidence worldwide. 6-Gingerol (6G) is a bioactive constituent of Zingiber officinale, which has been reported to possess various biological activities. This study was designed to evaluate the role of 6G in chronic UC. Chronic UC was induced in mice by three cycles of 2.5% dextran sulfate sodium (DSS) in drinking water. Each cycle consisted of 7 days of 2.5% DSS followed by 14 days of normal drinking water. 6G (100 mg/kg) and a reference anti-colitis drug sulfasalazine (SZ) (100 mg/kg) were orally administered daily to the mice throughout exposure to three cycles of 2.5% DSS. Administration of 6G and SZ significantly prevented disease activity index and aberrant crypt foci formation in DSS-treated mice. Furthermore, 6G and SZ suppresses immunoexpression of tumor necrosis factor alpha, interleukin-1ß, inducible nitric oxide synthase, Regulated on activation, normal T cell expressed and secreted (RANTES), and Monocyte chemoattractant protein-1 (MCP-1) in the DSS-treated mice. 6G effectively protected against colonic oxidative damage by augmenting the antioxidant status with marked decrease in lipid peroxidation levels in DSS-treated mice. Moreover, 6G significantly inhibited nuclear factor kappa B (P65), p38, cyclooxygenase-2, and ß-catenin whereas it enhanced IL-10 and adenomatous polyposis coli expression in DSS-treated mice. In conclusion, 6G prevented DSS-induced chronic UC via anti-inflammatory and antioxidative mechanisms and preservation of the Wnt/ß-catenin signaling pathway.

6-Gingerol improves testicular function in mice model of chronic ulcerative colitis.

The persistent inflammation and oxidative stress at the local site in ulcerative colitis reportedly extend to the testes via systemic circulation resulting in testicular dysfunction. The influence of 6-gingerol (6G), a phenolic compound isolated from Zingiber officinale, on colitis-mediated testicular dysfunction in mice was investigated in this study. Chronic ulcerative colitis was induced in mice using 2.5% dextran sulfate sodium (DSS) in drinking water for three cycles. Each cycle consisted of 7 consecutive days of exposure to DSS-treated water followed by 14 consecutive days of normal drinking water. 6G (100 mg/kg) or sulfasalazine (SZ; 100 mg/kg) was orally administered alone or in combination with DSS-treated water during the three cycles. SZ served as standard reference drug for colitis in this study. 6G significantly prevented the incidence of rectal bleeding, decrease in the body weight gain and colon mass index in DSS-exposed mice. 6G significantly prevented colitis-mediated decreases in luteinizing hormone, follicle-stimulating hormone and testosterone and decreases oxidative stress indices, pro-inflammatory cytokines and caspase-3 activity with concomitant augmentation of antioxidant enzymes activities, sperm characteristics, marker enzymes of testicular function and histoarchitecture in DSS-exposed mice. 6G exerted protective influence against ulcerative colitis-induced testicular damage via mechanisms involving its antioxidant and anti-inflammatory properties.

6-Gingerol-rich fraction prevents disruption of histomorphometry and marker enzymes of testicular function in carbendazim-treated rats.

Previous investigations demonstrated that 6-gingerol-rich fraction (6-GRF) prevented testicular toxicity via inhibition of oxidative stress and endocrine disruption in CBZ-treated rats. The influence of 6-GRF on alterations in histomorphometry and marker enzymes of testicular function in CBZ-treated rats which hitherto has not been reported was investigated in this study. The animals were orally administered either CBZ (50 mg/kg) alone or in combination with 6-GRF (50, 100 and 200 mg/kg) for 14 consecutive days. Histomorphormetric analysis demonstrated that 6-GRF significantly prevented CBZ-mediated increase in the organo-somatic index of the testes and seminiferous tubular diameter as well as the reduction in epithelium height and tubular length of testes in the rats. Similarly, 6-GRF ameliorated CBZ-induced disruption in the epithelium height as well as in the proportion of tubule and interstitium of the epididymis the treated rats. Furthermore, 6-GRF prevented CBZ-mediated increase in testicular acid phosphatase activity and the decrease in testicular alkaline phosphatase, aminotransferases, glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities. Moreover, 6-GRF ameliorated CBZ-induced reduction in the testicular and epididymal sperm count and sperm motility in the treated rats. Conclusively, 6-GRF enhances key functional enzymes involve in spermatogenesis and maintains histo-architecture of testes and epididymis in CBZ-treated rats.

6-Gingerol-rich fraction from Zingiber officinale ameliorates carbendazim-induced endocrine disruption and toxicity in testes and epididymis of rats.

This study evaluated the protective effects of 6-gingerol-rich fraction (6-GRF) from Zingiber officinale on carbendazim (CBZ)-induced reproductive toxicity in rats. Adult male rats were treated with either CBZ (50 mg/kg) alone or in combination with 6-GRF (50, 100 and 200 mg/kg) for 14 consecutive days. Gas chromatography-mass spectrometry (GCMS) analysis revealed that 6-GRF consists of ten bioactive chemical components with 6-gingerol being the most abundant (30.76%). Administration of 6-GRF significantly (p < .05) prevented CBZ-mediated increase in absolute and relative testes weights as well as restored the sperm quantity and quality in the treated rats to near control. In testes and epididymis, 6-GRF significantly abolished CBZ-mediated increase in oxidative damage as well as augmented antioxidant enzymes activities and glutathione level in the treated rats. Moreover, CBZ administration alone significantly decreased plasma levels of testosterone, thyrotropin, triiodothyronine and tetraiodothyronine, whereas follicle-stimulating hormone was significantly elevated without affecting luteinising hormone and prolactin levels when compared with the control. Conversely, 6-GRF ameliorated the disruption in the hormonal levels and restored their levels to near normalcy in CBZ-treated rats. Collectively, 6-GRF inhibited the adverse effects of CBZ on the antioxidant defence systems, hormonal balance and histology of the testes and epididymis in rats.

Insecticide chlorpyrifos and fungicide carbendazim, common food contaminants mixture, induce hepatic, renal, and splenic oxidative damage in female rats.

The fungicide carbendazim (CBZ) and insecticide chlorpyrifos (CPF) are currently applied together by farmers for the control of pests. Here, we investigated the impacts of 7 days oral co-exposure to 10 mg/kg body weight of CPF and 50 mg/kg body weight of CBZ on selected oxidative stress and antioxidant biomarkers in the liver, kidney, and spleen of female rats. The results showed that while the body weight gain and relative organ weights were not significantly affected after separate exposure to CPF and CBZ, there was a significant decrease in the body weight gain with concomitant increases in the relative kidney and spleen weights of rats treated with the mixture. Also, CPF and CBZ co-exposure significantly increased the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine ( p < 0.05) when compared with the groups treated with CBZ or CPF alone and the control. The significant decreases in both antioxidant enzymes activities and nonenzymatic antioxidant level following individual administration of CPF and CBZ to rats were intensified in the co-exposure group ( p < 0.05). Additionally, the marked increases in the levels of oxidative stress indices in liver, kidney, and spleen of rats treated with CPF or CBZ alone were intensified in the co-exposure group ( p < 0.05). Histopathologically, co-exposure to CPF and CBZ exacerbates their individual effects on the liver, kidney, and spleen. These findings showed that co-exposure to CPF and CBZ in rats elicited more severe oxidative damage on the liver, kidney, and spleen of the rats, indicative of an additive effect compared to CPF or CBZ alone and as such, may pose a greater environmental risk to humans.

Quercetin ameliorates polychlorinated biphenyls-induced testicular DNA damage in rats.

Polychlorinated biphenyls (PCBs) are a group of environmental contaminants widely reported to cause gonadal toxicity in both humans and animals. This study investigated the amelioratory role of quercetin in PCBs-induced DNA damage in male Wistar rats. Polychlorinated biphenyls were administered intraperitoneally at a dose of 2 mg kg(-1) alone or in combination with quercetin (orally) at 50 mg kg(-1) for 25 days. Quercetin modulation of PCBs-induced gonadal toxicity was evaluated using selected oxidative stress indices, comet assay, measurement of DNA concentration and histology of the testes. Administration of PCBs alone caused a significant (P < 0.05) depletion in the total thiol level in testes of treated rats. Conversely, the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) production were markedly elevated in testes of PCBs-treated rats compared with control. Further, PCBs exposure produced statistically significant increases in DNA tail migration, degraded double-stranded DNA (dsDNA) concentration and histological alterations of testes of the treated rats compared to control. Quercetin cotreatment significantly improved the testicular antioxidant status, decreased DNA fragmentation and restored the testicular histology, thus demonstrating the protective effect of quercetin in PCBs-treated rats.

Gallic acid protects against cyclophosphamide-induced toxicity in testis and epididymis of rats.

The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg(-1) for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg(-1) on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg(-1) ) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg(-1) for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione-S-transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA-treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone treated rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.

Artemisinin induces hormonal imbalance and oxidative damage in the erythrocytes and uterus but not in the ovary of rats.

Artemisinin is an antimalarial drug previously reported to induce neurotoxicity and embryotoxicity in animal models. This study investigated the erythrocytes and reproductive toxicity potentials of artemisinin in female rats. Animals were randomly divided into four study groups of eight rats each. The control group (group I) received corn oil, the vehicle, while groups II-IV were orally exposed to 7, 35 and 70 mg kg(-1) day(-1) of artemisinin, respectively, by gastric intubation for 7 consecutive days. Subsequently, we evaluated the impact of artemisinin on the endocrine environment and selected markers of oxidative damage and antioxidant status of the erythrocytes, ovary and uterus. Artemisinin significantly increased hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels and decreased catalase, glutathione peroxidase and superoxide dismutase activities in erythrocytes and uterus of rats compared with control group (p < 0.05). However, artemisinin did not alter ovarian MDA, H2O2, glutathione levels and catalase activity, while ovarian and uterine histological assessment revealed absence of visible lesions. Moreover, artemisinin significantly decreased follicle-stimulating hormone and increased progesterone levels compared with control (p < 0.05). Thus, these data suggest that in the absence of malarial parasite infection, artemisinin induced hormonal imbalance and oxidative damage in the erythrocytes and uterus but spared the ovary of rats.

Sperm characteristics, antioxidant status and hormonal profile in rats treated with artemisinin.

The indiscriminate use, abuse and patients' noncompliance to normal prescription of artemisinin and its derivatives are a common practice during the treatment for drug-resistant malaria parasites in most developing countries. This study investigated the influence of artemisinin on the testicular and epididymal sperm antioxidant systems as well as on the plasma levels of hormones from the pituitary and thyroid components of the brain-pituitary-testicular axis. Oral exposure of rats to 0, 7 and 35 mg kg(-1) artemisinin for 7 days showed that the testicular antioxidant status at both therapeutic dose (7 mg kg(-1) ) and overdose (35 mg kg(-1) ), and the sperm antioxidant status at therapeutic dose of artemisinin remained unaffected compared with control. However, increased hydrogen peroxide and lipid peroxidation levels were accompanied by a concomitant decrease in glutathione peroxidase and glutathione-S-transferase activities as well as glutathione level in spermatozoon of rats administered with overdose of artemisinin. While plasma levels of all the hormones investigated remained unaffected, severe epididymal degeneration with concomitant decrease in sperm quantity and quality was observed in rats treated with overdose of artemisinin compared with control. Overall, induction of oxidative stress in the epididymis, but not in the testes, could cause reproductive deficits in individuals unduly undergoing artemisinin therapy.

Kolaviron protects against ethylene glycol monoethyl ether-induced toxicity in boar spermatozoa.

This study investigated the ameliorative effects of kolaviron (a biflavonoid from the seed of Garcinia kola) and vitamin C on ethylene glycol monoethyl ether (EGEE)-induced oxidative damage in boar spermatozoa in vitro. EGEE (1.0 mm) was incubated with boar spermatozoa for 3 h with or without either kolaviron (50 and 100 µm) or vitamin C (1.0 mm). Spermatozoa parameters were determined hourly during the incubation period, whereas aminotransferases and alkaline phosphatase activities and oxidative stress indices were assessed after the incubation period. Results showed a time-dependent decline in spermatozoa motility and viability with significant elevation in total abnormalities in EGEE-treated spermatozoa. Exposure to EGEE resulted in significant increase in aminotransferases, alkaline phosphatase and superoxide dismutase (SOD) activities, whereas it markedly decreased glutathione (GSH) level, catalase (CAT) and glutathione S-transferase (GST) activities with concomitant increase in hydrogen peroxide (H2 O2 ) and malondialdehyde (MDA) levels. Pre-treatment of spermatozoa with kolaviron or vitamin C significantly decreased H2 O2 and MDA levels, improved spermatozoa characteristics and ameliorated oxidative damage in EGEE-treated spermatozoa. Taken together, EGEE exhibited its spermatotoxicity via induction of oxidative stress. The protective effects by kolaviron and vitamin C against EGEE-induced oxidative damage may be due to their intrinsic antioxidative potentials.

Kolaviron prevents carbendazim-induced steroidogenic dysfunction and apoptosis in testes of rats.

The study evaluated the protective role of kolaviron (an isolated biflavonoid from the seed of Garcinia kola) and vitamin E in carbendazim-induced reproductive dysfunction in male rats. Adult male Wistar rats were orally exposed to carbendazim (200mg/kg) singly or in combination with kolaviron (100 and 200mg/kg). Exposure to carbendazim significantly decreased the activities of superoxide dismutase and catalase but markedly increased sialic acid concentration and lipid peroxidation in the testes of rats. Western blot analysis revealed that carbendazim treatment decreased the expression of steroid acute regulatory (StAR) protein and androgen binding protein (ABP) with concomitant decrease in activities of steroidogenic enzymes. Germ cell apoptosis in carbendazim-treated rats was confirmed by TUNEL assay. However, pretreatment with kolaviron and vitamin E restored the testicular antioxidant status and steroidogenesis and decreased apoptotic nuclei to near control level in carbendazim-treated rats. Kolaviron may prove useful in combating carbendazim-induced reproductive toxicity.

Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether-induced pituitary-thyroid axis toxicity in male rats.

Endocrine disrupting chemicals cause reproductive dysfunction by interacting with intricate regulation and cellular processes involve in spermatogenesis. This study investigated the probable mechanism of action of ethylene glycol monoethyl ether (EGEE) as an antiandrogenic compound as well as the effects of kolaviron upon co-administration with EGEE in rats. Adult male rats were exposed to EGEE (200 mg kg(-1) bw) separately or in combination with either kolaviron [100 (KV1) and 200 (KV2) mg kg(-1) bw] or vitamin E (50 mg kg(-1) bw) for 14 days. Western blot analysis revealed that the administration of EGEE adversely affected steroidogenesis in experimental rats by decreasing the expression of steroid acute regulatory (StAR) protein and androgen-binding protein (ABP). EGEE significantly decreased the activities of 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and 17ß-hydroxysteroid dehydrogenase (17ß-HSD) but markedly increased sialic acid concentration in rat testes. EGEE-treated rats showed significant decreases in plasma levels of luteinising hormone (31%), testosterone (57.1%), prolactin (80.9%), triiodothyronine (65.3%) and thyroxine (41.4%), whereas follicle-stimulating hormone was significantly elevated by 76.9% compared to the control. However, co-administration of kolaviron or vitamin E significantly reversed the EGEE-induced steroidogenic dysfunction in rats. This study suggests that kolaviron may prove promising as a chemoprotective agent against endocrine pathology resulting from EGEE exposure.

Protective effects of kolaviron and quercetin on cadmium-induced testicular damage and endocrine pathology in rats.

This study evaluated the effects of kolaviron, a biflavonoid from Garcinia kola seed, and quercetin on cadmium-induced reproductive toxicity in rats. Adult male rats were administered with either cadmium (15 mg kg(-1)) alone or in combination with kolaviron (200 mg kg(-1)) or quercetin (10 mg kg(-1)) daily for 5 days. Cadmium-treated rats showed (P < 0.05) decrease in the body weight gain, testis and epididymis weights. However, upon co-administration of kolaviron or quercetin, these changes were significantly reversed in cadmium-treated rats. Also, administration of kolaviron or quercetin significantly prevented cadmium-mediated decrease in sperm motility and epididymal sperm concentration and reversed the increased level of sperm abnormality to near control. In testes and sperm, cadmium treatment resulted in significant decrease in the activities of superoxide dismutase, catalase and glutathione peroxidase, whereas it increased glutathione S-transferase activity as well as hydrogen peroxide and malondialdehyde levels. While plasma levels of triiodothyronine and tetraiodothyronine remained unaffected, the levels of testosterone, luteinising hormone and follicle stimulating hormone were decreased in cadmium-treated rats. Cadmium treatment caused mild congestion of interstitial vessels and oedema in the testes. Taken together, kolaviron and quercetin inhibited the adverse effects of cadmium on the antioxidant enzymes, markers of oxidative stress, endocrine and testicular structure in rats.

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.

Chemoprotection of ethylene glycol monoethyl ether-induced reproductive toxicity in male rats by kolaviron, isolated biflavonoid from Garcinia kola seed.

The present study investigated the protective effect of kolaviron, a biflavonoid from the seed of Garcinia kola, on ethylene glycol monoethyl ether (EGEE)-induced reproductive toxicity in male rats. The protective effect of kolaviron was validated using vitamin E, a standard antioxidant. EGEE was administered at a dose of 200 mg/kg. Other groups of rats were simultaneously treated with kolaviron (100 and 200 mg/kg) and vitamin E (50 mg/kg) for 14 days. EGEE treatment resulted in significant decrease in glutathione (GSH) level, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities but markedly increased the glutathione-S-transferase (GST) and lactate dehydrogenase (LDH) activities in the testes. In the spermatozoa, administration of EGEE caused significant decrease in the activities of CAT, GPx, GST and LDH as well as in the level of GSH but significantly increased SOD activity with concomitant increase in hydrogen peroxide and malondialdehyde levels in both testes and spermatozoa. EGEE-exposed rats showed marked testicular degeneration with concomitant decrease in spermatozoa quantity and quality. Overall, EGEE causes reproductive dysfunction in rats by altering antioxidant systems in the testes and spermatozoa. Kolaviron or vitamin E exhibited protective effects against EGEE-induced male reproductive toxicity by enhancement of antioxidant status and improvement in spermatozoa quantity and quality.

Nigerian bonny light crude oil induces irreversible reproductive toxicity in adult male rats.

BACKGROUND: The reversibility of reproductive toxicity induced by the Nigerian Bonny light crude oil (BLCO) was investigated in rats. METHOD: Adult male Wistar rats were orally treated with BLCO at 0, 50, 100 and 200mg kg(-1) for 21 days. One-half of the rats were sacrificed on day 22 while the remaining one-half stayed additional 21 days without treatment. RESULTS: While sperm quality was compromised in dose-dependent manner, testis histopathology was only evident at 200 mg kg(-1) after 21 days. BLCO significantly decreased activities of superoxide dismutase, catalase and glucose-6-phosphate dehydrogenase but markedly elevated gamma glutamyltransferase and glutathione S-transferase activities as well as malondialdehyde, hydrogen peroxide and glutathione levels in both testes and sperm. Most of the above-mentioned parameters were consistent in animals from withdrawal experiment. CONCLUSION: Taken together, BLCO exposure impaired fertility via increased oxidative stress and was not reversible upon withdrawal of treatment within the time course of investigation in male rats. BLCO exposure poses a risk for impaired fertility and its contribution to infertility in the Nigerian male population may not be excluded.

Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice.

The present study investigated the effects of aflatoxin B1 (AFB1) and ethanol co-exposure on biomarkers of hepatic damage in mice. Four groups of adult male mice were treated for 7 consecutive days. Control mice received corn oil alone at a dose of 2 mL/kg bw. One group was treated with ethanol at a dose of 500 µL/kg bw and another group administered 9 mg/kg bw of AFB1 dissolved in corn oil. The fourth group was co-administered with ethanol and AFB1. The body and liver weights of treated mice decreased significantly when compared with corresponding control. Alone, ethanol and AFB(1) treatment separately increased serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP). Alcohol dehydrogenase (ALD) activity was markedly elevated in ethanol-treated mice but was unaffected by AFB1 treatment. Co-exposure of AFB1 and ethanol escalated the activities of these serum enzymes. Administration of ethanol and AFB1 separately resulted in significant decrease in both non-enzymatic antioxidant glutathione (GSH) level and enzymatic antioxidant catalase (CAT) and glutathione-S-transferase (GST) activities, whereas lipid peroxidation was markedly elevated. Superoxide dismutase activity and vitamin C level remained unaffected in all treatment groups. Co-exposure of animals to ethanol and AFB1 showed additive effects on the activities of GST and CAT as well as on the GSH level. Histopathological study revealed that these compounds interact together to exacerbate their individual effects on the liver. In summary, the data presented showed that AFB1 and ethanol co-exposure induced severe oxidative damage to the liver of mice and as such humans consuming excessive amount of ethanol and diets contaminated with AFB1 simultaneously may be at greater risk of the hepatotoxic effects of these compounds.

Evaluation of antioxidant properties of Mallotus oppositifolium in in-vitro, in-vivo and ex-vivo model systems.

The protective effect of antioxidants and naturally occurring substances against oxidative stress damage has recently attracted much attention. The leaves of Mallotus oppositifolium, a shrub of the family Euphorbiacea that grows in many parts of Africa, are used in folk medicine and herbal preparations for the treatment of dysentery, worms and malaria. The study investigated the antioxidant properties of the methanolic extract of the leaves of Mallotus oppositifolium (MEMO) in comparison with butylated hydroxyl anisole (BHA) as a standard antioxidant using three free radical generators viz hydrophilic radical generator 2,2-azobis(2-amidino propane) dihydrochloride (AAPH), hydrophobic radical generator 2,2-azobis(2,4-dimethylvaleronitrile) (AMVN) and hydroxyl radical and non-specific radical generator Fe2+/ascorbate system in an in vitro, in vivo and ex-vivo model systems. Phytochemical analysis of the leaves extract was also assessed. Phytochemical analysis of the powdered leaves revealed the presence of alkaloids, tannins, cardenolides and saponins. In vitro study indicated that while MEMO failed to inhibit lipid peroxidation (LPO) induced by AAPH, while BHA offered 55.5% inhibition. In addition, while AMVN-induced LPO was inhibited by 17.7% and 29.4% by MEMO and BHA respectively, Fe2+/ascorbate system-induced LPO was inhibited by 57.9% and 78.9% by MEMO and BHArespectively. Ex-vivo studies showed that MEMO at 100mg/kg bw reduced malondialdehyde and protein carbonyl levels by 34.5% and 12.0% respectively compared with the control. In vivo, MEMO increased (P<0.05) superoxide dismutase and catalase activities by 408.0% and 295.0% respectively. Taken together, this study demonstrates that MEMO exhibits antioxidant, radical scavenging and enhancement of enzymatic antioxidant capacity and as such could intervene in toxicological processes mediated by free radical mechanisms.

Influence of quercetin on haematological indices and biomarkers of oxidative stress in the serum of rats exposed to atrazine.

The study was carried out to compare the effects of quercetin (QT) at doses of 5mg/kg (Q5) and 10mg/kg (Q10) against the hematological toxicity and oxidative stress caused by atrazine (ATR). Male rats were orally gavaged with ATR at a dose of 120mg/kg for 16 days. Erythropenia, leucopenia was observed in ATR treated rats. Other hematological variables such as packed cell volume (PCV), hemoglobin concentration (HGB), mean cell hemoglobin concentration (MCHC), mean corpuscular volume (MCV), neutrophils (NEU), lymphocytes (LYM) and blood platelet (PLT) showed no significant change with respect to the control values. The activities of the antioxidant defense molecules including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) and glutathione (GSH) were decreased; malondialdehyde (MDA) level increased but catalase (CAT) activity showed no change.Co-administration of Q5 did not prevent the oxidative stress and the hematological alterations caused by ATR. In these groups of animals, the values of PLT and NEUT were increased while LYM decreased indicating more pronounce hematological changes. The changes in both the biochemical and hematological variables were normalized to the control values on co-administration of Q10. We suggest that the antioxidant activities of QT at a doses of 10mg/kg could be responsible for its protective effects against ATR-induced oxidative stress and hematological toxicity.