Hydro-Ethanolic Fruit Extract of Capsicum frutescens Reversed Triton-X-100-Induced Hyperlipidaemia in Rats.

This study evaluates the anti-hyperlipidaemic and antioxidant activities of hydro-ethanolic fruits extract of Capsicum frutescens in hyperlipidemia rats. The secondary volatile metabolite constituents of the extract were identified using Gas chromatography. In vitro antioxidant activity of the extract (0.2-1.0 mg/mL) was investigated using 2, 2-diphenyl-1-picrylhydrazyl (DPPH) radical, hydrogen peroxide (H2O2) and hydroxyl radical (OH.). In vivo antioxidant and anti-hyperlipidaemic properties of the extract were evaluated in triton X-100-induced hyperlipidaemic rats. Gas chromatogram indicates the presence of 13 compounds with tans ß-ocimene being the major constituent. The extract scavenged DPPH, H2O2 and OH. radicals in concentrations dependent manner. C. frutescens reversed triton X-100-mediated increase in serum total cholesterol, triglycerides and low-density lipoprotein, and reduction in high-density lipoprotein. Triton X-100-mediated decrease in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phospahte dehydrogenase were significantly reversed by the extract. The results indicate that C. frutescens has antioxidant and anti-hyperlipidaemic properties.

Loperamide-induced cardiotoxicity in rats: Evidence from cardiac and oxidative stress biomarkers.

At therapeutic dose, loperamide is a safe over-the-counter antidiarrheal drug but could induce cardiotoxic effect at a supratherapeutic dose. In this study, we use cardiac and oxidative biomarkers to evaluate loperamide-induced cardiotoxicity in rats. Rats were orally gavaged with 1.5, 3, or 6 mg/kg body weight (BW) of loperamide hydrochloride for 7 days. The results after 7 days administration of loperamide, revealed dose-dependent increase (P < 0.05) in aspartate aminotransferase, lactate dehydrogenase, creatine kinase-MB, and serum concentration of cardiac troponin I, total homocysteine, and nitric oxide. A 50% decrease in antioxidant enzymes activity was observed at 6 mg/kg BW. Furthermore, malondialdehyde and fragmented DNA also increased significantly in the heart of the treatment groups. Loperamide provoked cardiotoxicity through oxidative stress, lipid peroxidation, and DNA fragmentation in rats. This study has provided a possible biochemical explanation for the reported cardiotoxicity induced by loperamide overdose.

Menadione perturbs oxidative stress biomarkers and testicular function indices of rats.

In this study, we evaluated the influence of menadione on the androgenic, oxidative stress biomarkers, and testicular function indices in rats. Rats (20) were randomized into four groups (A-D) of five rats each. Rats in groups A, B, C, and D received the vehicle of administration (olive oil), 25, 50, or 100 mg/kg body weight menadione intraperitoneally, respectively, for 7 days. Menadione lowered serum cholesterol, follicle-stimulating hormone, luteinizing hormone, and testosterone and luteinizing hormone reduced significantly in rats when compared with the control rats. Furthermore, menadione lowered the testicular function indices in the testes of rats. The activities of superoxide dismutase and catalase in the testes of menadione-treated rats decreased significantly. Also, glutathione was depleted with concomitant malondialdehyde increase. The findings of this study show that menadione induces testicular toxicity by depleting the antioxidant defense system leading to perturbation in the testicular function indices.

Contributions of RecA and RecBCD DNA repair pathways to the oxidative stress response and sensitivity of Acinetobacter baumannii to antibiotics.

OBJECTIVES: RecA and RecBCD are responsible for the repair of oxidative DNA damage in bacteria, including Acinetobacter baumannii (A. baumannii). This study evaluated the contribution of recA, recB, recC and recD to the sensitivity and oxidative response of A. baumannii to antibiotics. RESULTS: Inactivation of recA, recB, recC and recD significantly increased the susceptibility of A. baumannii AB5075 to colistin, gentamicin, rifampicin and tigecycline. Furthermore, superoxide anion radicals (•O2-) and hydrogen peroxide (H2O2) accumulated in colistin, gentamicin, rifampicin or tigecycline-treated ΔrecA, ΔrecB, ΔrecC and ΔrecD mutants compared with the parental strain. Concomitantly, a more pronounced increase in fragmented DNA was observed in the mutants compared with the parental strain upon antibiotic treatment. Chelation of ferrous ion (Fe2+) with dipyridyl lowered the susceptibility of ΔrecA, ΔrecB, ΔrecC and ΔrecD strains of A. baumannii to colistin, gentamicin and rifampicin, but not tigecycline, to a level comparable with the parental strain. Antibiotic-mediated accumulation of reactive oxygen species depleted glutathione, with a more profound response in the mutants compared with the parental strain. The antibiotics, except tigecycline, raised the oxidized nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide and adenosine diphosphate/adenosine triphosphate ratio of ΔrecA, ΔrecB, ΔrecC and ΔrecD mutants compared with the parental strain. CONCLUSION: Reduced capability of ΔrecA, ΔrecB, ΔrecC and ΔrecD mutants to repair DNA raised the susceptibility of A. baumannii to colistin, gentamicin, rifampicin and tigecycline. The available data further support the notion that oxidative stress contributes to antibiotic-mediated bacterial killing.

Lophirones B and C halt acetaminophen hepatotoxicity by upregulating redox transcription factor Nrf-2 through Akt, PI3K, and PKC pathways.

We investigated the mechanism of lophirones B- and C-mediated protection against acetaminophen hepatotoxicity. Mice were pretreated with 20 mg/kg body weight lophirones B and C for 7 days and challenged with acetaminophen on day 7. Acetaminophen raised nuclear factor-κB (NF-κB) in the liver of mice but lowered protein kinase B (Akt). Although, acetaminophen produced no significant alteration on nuclear erythroid related factor-2 (Nrf-2), phosphoinositide 3-kinase (PI3K) and protein kinase C (PKC), lophirones B and C raised the level of these proteins and Akt. The acetaminophen-mediated increase in NF-κB was significantly reversed by lophirones B and C. Lophirones B and C prevented acetaminophen-mediated alterations in serum biomarkers of hepatic injury. Similarly, lophirones B and C lowered the biomarkers of oxidative stress in the liver of acetaminophen-treated mice. It can be inferred from this study that lophirones B and C prevent acetaminophen-induced liver injury by enhancing Nrf-2 through Akt, PI3K, and PKC pathways.

Phenolic acids potentiate colistin-mediated killing of Acinetobacter baumannii by inducing redox imbalance.

Phenolic acids with catechol groups are good prooxidants because of their low redox potential. In this study, we provided data showing that phenolic acids, caffeic acid, gallic acid and protocatechuic acid, enhanced colistin-mediated bacterial death by inducing redox imbalance. The minimum inhibitory concentrations of these phenolic acids against Acinetobacter baumannii AB5075 were considerably lowered for ΔsodB and ΔkatG mutants. Checkerboard assay shows synergistic interactions between colistin and phenolic acids. The phenolic acids exacerbated colistin-induced oxidative stress in A. baumannii AB5075 through increased superoxide anion generation, NAD + /NADH and ADP/ATP ratio. In parallel, the level of reduced glutathione was significantly lowered. We conclude that phenolic acids potentiate colistin-induced oxidative stress in A. baumannii AB5075 by increasing ROS generation, energy metabolism and electron transport chain activity with a concomitant decrease in glutathione.

Dietary phenolic acids reverse insulin resistance, hyperglycaemia, dyslipidaemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome rats.

This study investigated the influence of caffeic, ferulic, gallic and protocatechuic acids on high-fructose diet-induced metabolic syndrome in rats. Oral administration of the phenolic acids significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, phenolic acids restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Similarly, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of phenolic acids restored High-fructose diet-mediated increase in the levels of lipid parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. The result of this study shows protective influence of caffeic acid, ferulic acid, gallic acid and protocatechuic acid in high-fructose diet-induced metabolic syndrome.

Hepatoprotective potential of Phyllanthus muellarianus leaf extract: studies on hepatic, oxidative stress and inflammatory biomarkers.

CONTEXT: Leaves of Phyllanthus muellarianus (Kuntze) Exell. (Euphorbiacea) are widely used in the management of liver disorders in Nigeria. However, no there is no scientific validation to support this use. OBJECTIVE: Hepatoprotective effect of Phyllanthus muellarianus aqueous leaf extract was investigated in acetaminophen-induced liver injury mice. MATERIALS AND METHODS: Hepatoprotective effect of Phyllanthus muellarianus aqueous leaf extract was evaluated in acetaminophen-induced hepatic damage in Swiss albino mice using biomarkers of hepatocellular indices, oxidative stress, proinflammatory factors and lipid peroxidation. Mice received distilled water, 100, 200, or 400 mg/kg b.w of Phyllanthus muellarianus aqueous leaf extract, respectively, for seven days. Treatment groups were challenged with 300 mg/kg b.w of acetaminophen on the sixth day. RESULTS: Oral administration of Phyllanthus muellarianus aqueous leaf extract significantly (p < 0.05) attenuates acetaminophen-mediated alterations in serum alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, albumin and total bilirubin by 76.56, 85.41, 89.39, 82.77 and 78.38%. Similarly, acetaminophen-mediated decrease in activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase were significantly attenuated in the liver of mice by 85.10, 80.81, 80.45, 76.23 and 95.22%, respectively. Increased levels of conjugated dienes, lipid hydroperoxides, malondialdehyde, protein carbonyl, fragmented DNA, tumor necrosis factor-α, interleukin-6 and -8 were significantly lowered by Phyllanthus muellarianus aqueous leaf extract. CONCLUSION: Overall, results of this study show that Phyllanthus muellarianus halted acetaminophen-mediated hepatotoxicity due to its capability to enhance antioxidant enzymes.

Involvement of oxidative stress in protocatechuic acid-mediated bacterial lethality.

The involvement of oxidative stress in protocatechuic acid-mediated bacterial lethality was investigated. Minimum inhibitory concentrations (MIC) and minimum bactericidal concentration (MBC) of protocatechuic acid against Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus are 600 and 700 µg/ml, 600 and 800 µg/ml, and 600 and 800 µg/ml, respectively. The optical densities and colony-forming units of protocatechuic acid-treated bacteria decreased in time-dependent manner. Protocatechuic acid (4× MIC) significantly increased the superoxide anion content of E. coli, P. aeruginosa, and S. aureus compared to dimethyl sulfoxide (DMSO). Superoxide dismutase, catalase, and NAD+ /NADH in protocatechuic acid-treated E. coli, P. aeruginosa, and S. aureus increased significantly when compared to DMSO. Conversely, level of reduced glutathione decreased in protocatechuic acid-treated E. coli, P. aeruginosa, and S. aureus, while glutathione disulfide increased when compared to DMSO. Furthermore, malondialdehyde and fragmented DNA increased significantly following exposure to protocatechuic acid. Protocatechuic acid inhibited the activity of complexes I and II. From the above findings, protocatechuic acid enhanced the generation of reactive oxygen species (superoxide anion radical and hydroxyl radical) in E. coli, P. aeruginosa, and S. aureus, possibly by autoxidation, fenton chemistry, and inhibiting electron transport chain resulting in lipid peroxidation and DNA fragmentation and consequentially bacterial cell death.

Lophirones B and C Attenuate Acetaminophen-Induced Liver Damage in Mice: Studies on Hepatic, Oxidative Stress and Inflammatory Biomarkers.

Lophirones B and C are chalcone dimers with proven chemopreventive activity. This study evaluates the hepatoprotective effect lophirones B and C in acetaminophen-induced hepatic damage in mice using biomarkers of hepatocellular indices, oxidative stress, proinflammatory factors and lipid peroxidation. Oral administrations of lophirones B and C significantly (p < 0.05) attenuated acetaminophen-mediated alterations in serum alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, albumin and total bilirubin. Similarly, acetaminophen-mediated decrease in activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6- phosphate dehydrogenase were significantly attenuated in the liver of mice. Increased levels of conjugated dienes, lipid hydroperoxides, malondialdehyde, protein carbonyl and fragmented DNA were significantly lowered by lophirones B and C. Levels of tumour necrosis factor-α, interleukin-6 and 8 were significantly lowered in serum of acetaminophen treated mice by the chalcone dimers. Overall, results of this study show that lophirones B and C halted acetaminophen-mediated hepatotoxicity.

Hibiscus sabdariffa calyx palliates insulin resistance, hyperglycemia, dyslipidemia and oxidative rout in fructose-induced metabolic syndrome rats.

BACKGROUND: The effect of Hibiscus sabdariffa calyx extract was evaluated in high-fructose-induced metabolic syndrome rats. Insulin resistance, hyperglycemia, dyslipidemia and oxidative rout were induced in rats using high-fructose diet. High-fructose diet-fed rats were administered 100 and 200 mg kg(-1) body weight of H. sabdariffa extract for 3 weeks, starting from week 7 of high-fructose diet treatment. RESULTS: High-fructose diet significantly (P < 0.05) increased the serum levels of blood glucose, insulin, total cholesterol (TC), triacylglycerol (TAG), low-density lipoprotein cholesterol (LDLc) and very-low-density lipoprotein cholesterol (VLDLc), with a concomitant reduction in high-density lipoprotein cholesterol (HDLc). These alterations were significantly ameliorated by the extract. High-fructose diet-mediated decreases in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GSH-red) and glucose 6-phosphate dehydrogenase (Glc 6-PD) were significantly (P < 0.05) attenuated. Altered levels of reduced glutathione (GSH) and glutathione disulfide (GSSG) were significantly (P < 0.05) restored to normal. High-fructose diet-mediated increases in the concentrations of malondialdehyde, conjugated dienes, lipid hydroperoxides, protein carbonyl and percentage fragmented DNA were significantly (P < 0.05) lowered by the Hibiscus extract. CONCLUSION: Overall, aqueous extract of H. sabdariffa palliates insulin resistance, hyperglycemia, dyslipidemia and oxidative rout in high-fructose-induced metabolic syndrome rats.

A fermented sorghum/millet-based beverage, Obiolor, extenuates high-fat diet-induced dyslipidaemia and redox imbalance in the livers of rats.

BACKGROUND: Obiolor, a non-alcoholic beverage produced from fermented sorghum and millet malts, is widely consumed on a daily basis by the Igala tribe in Nigeria and is closely associated with good health. The effect of Obiolor on dyslipidaemia, protein oxidation, lipid peroxidation and DNA fragmentation in the liver of rats fed a high-fat diet was investigated. RESULTS: High-fat diet-mediated alterations in liver and serum total cholesterol, triacylglycerol, high-density lipoprotein cholesterol, low-density cholesterol and very low-density lipoprotein cholesterol were significantly (P < 0.05) reversed by Obiolor. The beverage increased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase in the liver of rats. These increases significantly (P < 0.05) attenuated the high-fat diet-mediated decrease in antioxidant enzymes. High-fat diet-mediated elevations in the levels of conjugated dienes, lipid hydroperoxides, malondialdehyde, protein carbonyl and DNA fragmentation in the livers of rats were lowered by the beverage. CONCLUSION: This study showed that Obiolor extenuated high-fat diet-mediated dyslipidaemia, protein oxidation, lipid peroxidation and DNA fragmentation in rats.

Aqueous root extract of Lecaniodiscus cupanioides restores nitric oxide/cyclic guanosine monophosphate pathway in sexually impaired male rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Aqueous root extract of Lecaniodiscus cupanioides is widely used in the management of sexual dysfunction in Nigeria. The effect of aqueous root extract of L. cupanioides root on the concentrations of penile cyclic Guanosine Monophosphate (cGMP) and plasma nitric oxide in paroxetine-induced sexually impaired male rats was evaluated. METHODS: Thirty (30) albino rats were assigned into six groups (A, B, C, D, E and F) of five rats each such that animals in Group A (control) received distilled water while those in Groups B, C, D, E and F which were induced into sexual dysfunction (p.o 10mg/kg of paroxetine hydrochloride suspension in Tween-80) and in addition received distilled water, 7.14 mg/kg body weight of a reference herbal drug (PowmaxM), 25, 50 and 100mg/kg body weight of the extract respectively, orally, once daily for five days. RESULTS: Administration of paroxetine significantly reduced the levels of penile cyclic Guanosine Monophosphate (cGMP) and plasma nitric oxide. These decreases were dose dependently reversed by the aqueous extract of L. cupanioides root. The reversal by the 25 and 50mg/kg body weight of the extract compared favorably with the PowmaxM, whereas the 100mg/kg body weight of the extract compared favorably with the non-sexually impaired distilled water treated control animals. CONCLUSION: The results of this study show that aqueous extract of L. cupanioides root restored the levels of cGMP and nitric oxide in sexually impaired rats. This study further lends credence to the use of aqueous root extract of L. cupanioides in the management of sexual dysfunction in Nigeria.

Anti-ulcerogenic activity of aqueous extract of Carica papaya seed on indomethacin-induced peptic ulcer in male albino rats.

OBJECTIVE: Carica papaya is an important fruit with its seeds used in the treatment of ulcer in Nigeria. This study investigated the anti-ulcerogenic and antioxidant activities of aqueous extract of Carica papaya seed against indomethacin-induced peptic ulcer in male rats. METHODS: Thirty male rats were separated into 6 groups (A-F) of five rats each. For 14 d before ulcer induction with indomethacin, groups received once daily oral doses of vehicle (distilled water), cimetidine 200 mg/kg body weight (BW), or aqueous extract of C. papaya seed at doses of 100, 150 or 200 mg/kg BW (groups A, B, C, D, E and F, respectively). Twenty-four hours after the last treatment, groups B, C, D, E and F were treated with 100 mg/kg BW of indomethacin to induce ulcer formation. RESULTS: Carica papaya seed extract significantly (P< 0.05) increased gastric pH and percentage of ulcer inhibition relative to indomethacin-induced ulcer rats. The extract significantly (P< 0.05) decreased gastric acidity, gastric acid output, gastric pepsin secretion, ulcer index and gastric secretion volume relative to group B. These results were similar to that achieved by pretreatment with cimetidine. Specific activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase in the extract-treated groups (D, E and F) were increased significantly over the group B (P< 0.05). Pretreatment with the seed extract protected rats from the indomethacin-mediated decrease in enzyme function experienced by the group B. Similarly, indomethacin-mediated decrease in reduced glutathione level and indomethacin-mediated increase in malondialdehyde were reversed by Carica papaya extract. CONCLUSION: In this study, pretreatment with aqueous extract of Carica papaya seed exhibited anti-ulcerogenic and antioxidant effects, which may be due to the enhanced antioxidant enzymes.

Combined administration of silymarin and vitamin C stalls acetaminophen-mediated hepatic oxidative insults in Wistar rats

Oxidative insult by free radicals has been implicated in drug-induced hepatic damage and this has resulted in frequent episodes of liver disorders. Therapeutic efficacy of antioxidants may provide a possible solution to this menace. This study was carried out to investigate the effect of combined administration of silymarin and vitamin C in rescuing acetaminophen-induced hepatotoxicity in rats. Hepatotoxic rats were orally administered with silymarin and vitamin C at 100 and 200 mg/kg body weight, respectively. At the end of the experiment, liver function indices, antioxidant parameters and histological analysis were evaluated. We observed that the significantly increased (p < 0.05) activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, as well as levels of thiobarbituric acid reactive substances and serum total bilirubin, were markedly reduced following co-administration of silymarin and vitamin C. The compounds also effectively reversed the reduced activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase and total protein concentration in the hepatotoxic rats. These findings are indicative of hepatoprotective and antioxidant attributes of the two compounds which are also supported by the histological analysis. The available evidences in this study suggest that the complementary effects of silymarin and vitamin C proved to be capable of ameliorating acetaminophen-mediated hepatic oxidative damage and the probable mechanism is via antioxidative action.

Effects of trona on the redox status of cellular system of male rats.

The effects of trona (Kaun), a food additive, on the redox status of the liver and kidney of male Wistar rats were investigated. A total of 60 male rats (145 ± 2.52 g) were grouped into four: A, B, C and D, where group A (the control) received 1 mL of distilled water orally while those in groups B, C and D (test groups) received orally, same volume of trona preparation corresponding to 100, 200 and 400 mg/kg body weight, respectively, for 28 days. Administration of trona significantly reduced (p < 0.05) alkaline phosphatase activity in the liver and kidney with corresponding increases in the serum enzyme. Acid phosphatase activity increased significantly (p < 0.05) in the liver and kidney with no significant change (p > 0.05) in the activity of the serum enzyme. The activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and the levels of reduced glutathione, vitamins C and E in the liver and kidney of the animals decreased significantly (p < 0.05). In contrast, malondialdehyde and lipid hydroperoxide of trona-treated animals increased significantly (p < 0.05) in liver and kidney. Overall, data from this study revealed that trona exhibited its toxic effect by suppressing or depleting the antioxidant systems and increasing the risk of attack by oxidants generated either from its metabolites or from other in vivo means on the rat cellular system.

Sorghum-based alcoholic beverage, Burukutu, perturbs the redox status of the liver of male rats.

The redox status of male rat liver following 28 days consumption of Burukutu was investigated. Twenty rats were randomized into four groups with five rats each. Burukutu consumption at 0.78 g/kg alcohol produced no significant change in the activities of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). However, 3.71 and 7.43 g/kg dosages resulted in significant decrease in the activities of ALP, ALT and AST with corresponding increase in serum. The activity of cytochrome P450(CYP 2E1) increased significantly in the liver of rats following consumption of Burukutu at all doses investigated. The activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase decreased significantly (P < 0.05) in rats treat with 0.78 g/kg, 3.41 and 7.43 g/kg Burukutu. There was a significant increase in the level of glutathione disulfide (GSSG) with reduction in the levels of glutathione reduced (GSH) and GSH:GSSG. The levels of oxidative stress biomarkers, malondialdehyde, conjugated dienes, lipid hydroperoxides, protein carbonyl and percentage DNA fragmentation, increased significantly (P < 0.05). It is evident from the alterations in the activities of the hepatocellular enzymes, antioxidant enzymes and oxidative stress biomarkers that Burukutu mediated its toxicity through the depletion of the antioxidant enzymes.

Nutritional and antioxidant dispositions of sorghum/millet-based beverages indigenous to Nigeria.

Sorghum/millet-based beverages, Obiolor and Pito, were evaluated for their nutritional and antioxidant dispositions. Analyzed Obiolor and Pito contained 96% and 97% moisture; 7.8% and 3.7% crude protein; 8.9% and 5.6% available carbohydrate; 0.39% and 0.31% crude fat; 0.3% and 0.2% crude fiber; 2.4% and 1.5% ash; and 459.3 and 164 kJ/g energy value, respectively. Obiolor and Pito (1.0 mL) scavenged 2,2-diphenyl-1-picrylhydrazyl by 87% and 81%; superoxide ion by 65% and 59%; hydrogen peroxide by 79% and 76%; and hydroxyl radical by 82% and 85%, respectively. The beverages significantly reduced ferric ion. Aflatoxin B1-mediated increase in lipid peroxidation products (conjugated dienes, lipid hydroperoxides, and malondialdehydes) and protein carbonyl in the microsomes were significantly (P < 0.05) reduced by the beverages. The data obtained from this study show that the sorghum-based beverages (Obiolor and Pito) can serve as functional foods, as evident from their antioxidant capabilities in addition to their gross energy content.

Phenolic extract of Parkia biglobosa fruit pulp stalls aflatoxin B1 – mediated oxidative rout in the liver of male rats

The effect of phenolic extract of Parkia biglobosa (Jacq.) R. Br. ex G. Don, Fabaceae, pulp on aflatoxin B1 induced oxidative imbalance in rat liver was evaluated. Thirty-five male rats were randomized into seven groups of five animals each. Rats in group A served as control and received vehicle for drug administration (0.5% DMSO) once daily at 24 h intervals for six weeks. Rats in groups B, D, E, F and G, received aflatoxin B1 (167 μg/kg body weight) in 0.5% DMSO for three weeks, starting from the third week of the experimental period. Rats in Group C received 400 mg/kg bodyweight of the extract for six weeks, while groups D, E and F rats were treated with 100, 200 and 400 mg/kg bodyweight of the extract for six weeks respectively. Group G rats received 100 mg/kg body weight of vitamin C. Aflatoxin B1-mediated decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase were significantly attenuated. Aflatoxin B1 mediated the elevation in malondialdehyde, conjugated dienes, lipid hydroperoxides, protein carbonyl, and significantly lowered DNA fragmentation percentage. Overall, the phenolic extract of P. biglobosa pulp stalls aflatoxin B1-mediated oxidative rout by enhancing antioxidant enzyme activities leading to decreased lipid peroxidation, protein oxidation and DNA fragmentation.

Lophirones B and C extenuate AFB1-mediated oxidative onslaught on cellular proteins, lipids, and DNA through Nrf-2 expression.

The capability of lophirones B and C to extenuate aflatoxin B1 (AFB1)-mediated onslaught on cellular proteins, lipids, and DNA was investigated for 6 weeks. Lophirones B and C significantly (P < 0.05) increase the expression and specific activity of cytoprotective enzymes (glutathione-S-trans-ferase, nioctinamide adenine dicludeotide:quinone oxidoreductase-1, epoxide hydrolase, and uridyl glucuronosyl transferase). There was significant (P < 0.05) reduction in the level of antioxidant system in AFB1-induced hepatocarcinogenesis. Furthermore, lophirones B and C significantly (P < 0.05) attenuated AFB1-mediated decrease in the specific activities of antioxidant enzymes. Oxidative stress biomarkers, malondialdehyde, lipid hydroperoxides, conjugated dienes, protein carbonyl, and fragmented DNA were significantly (P < 0.05) elevated in AFB1-treated rats. Although lophirones B and C did not significantly (P < 0.05) alter these biomarkers, an AFB1-mediated increase in these biomarkers was significantly attenuated. Results obtained showed that lophirones B and C extenuate AFB1-mediated onslaught on cellular proteins, lipids, and DNA by enhancing nuclear erythroid-related factor-2 expression.