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PubMed1996

Characterization of a chemical anoxia model in cerebellar granule neurons using sodium azide: protection by nifedipine and MK-801.

Induction of chemical anoxia, using sodium azide in cerebellar granule cells maintained in primary culture, was evaluated as an in vitro assay for screening of potential neuroprotective compounds. The purpose of this study was to evaluate sodium azide as an alternative to cyanide salts, compounds which, despite their unfavorable characteristics, are often used in assays for chemical anoxia. The viability of neuronal cultures after treatment with azide, with or without preincubation with calcium channel blockers, tetrodotoxin (TTX), or glutamate receptor antagonists, was monitored by subsequent incubation with the tetrazolium dye MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), followed by isopropanol extraction and spectrophotometric quantification of cellularly reduced MTT. The azide-induced degeneration of neurons was shown to be dependent on the concentration as well as on the duration of incubation with submaximal concentrations of azide. Incubation of the neurons with nifedipine, a blocker of L-type voltage-sensitive calcium channels (L-VSCC), or with the noncompetitive N-methyl-D-aspartate (NMDA) subtype glutamate receptor antagonist MK-801, prior to addition of submaximal concentrations of azide, significantly attenuated azide-induced neuronal death. Blockers of N-type and Q-type VSCC (omega-conotoxin MVIIA and MVIIC, respectively) and the P-type VSCC blocker omega-agatoxin IVA had no effect in this assay. The sodium channel blocker TTX was without effect when added to neurons under depolarizing conditions, but potently and effectively protected cells when experiments were performed in a nondepolarizing buffer. The results show that chemical anoxia induced by incubation of cultured neurons with azide leads to detrimental effects, which may be quantitatively monitored by the capability of the cells to reduce MTT. This procedure is a suitable method for screening of compounds for possible protective effects against neuronal death induced by energy depletion. In addition, the results suggest involvement of L-type VSCC as well as of glutamate receptors in the pathways leading to neuronal degradation induced by energy depletion in cerebellar granule neurons. This would further support the notion that these pathways might be important in neurodegeneration induced by cerebral ischemia or anoxia.

Animals↗
PubMed2002

Parenteral iron formulations: a comparative toxicologic analysis and mechanisms of cell injury.

BACKGROUND: Multiple parenteral iron (Fe) formulations exist for administration to patients with end-stage renal disease. Although there are concerns regarding their potential toxicities, no direct in vitro comparisons of these agents exist. Thus, the present study contrasted pro-oxidant and cytotoxic potentials of four available Fe preparations: Fe dextran (Fe dext), Fe sucrose (Fe sucr), Fe gluconate (Fe gluc), and Fe oligosaccharide (Fe OS). METHODS: Differing dosages (0.06 to 1 mg/mL) of each compound were added to either (1) isolated mouse proximal tubule segments, (2) renal cortical homogenates, or (3) cultured human proximal tubule (HK-2) cells (0.5- to 72-hour incubations). Oxidant injury (malondialdehyde generation) and lethal cell injury (percentage of lactate dehydrogenase release; tetrazolium dye uptake) were assessed. Effects of selected antioxidants (glutathione [GSH], catalase, dimethylthiourea (DMTU), and sodium benzoate also were assessed. RESULTS: Each test agent induced massive and similar degrees of lipid peroxidation. Nevertheless, marked differences in cell death resulted (Fe sucr >> Fe gluc > Fe dext approximately Fe OS). This relative toxicity profile also was observed in cultured aortic endothelial cells. Catalase, DMTU, and sodium benzoate conferred no protection. However, GSH and its constituent amino acid glycine blocked Fe sucr-mediated cell death. The latter was mediated by mitochondrial blockade, causing free radical generation and a severe adenosine triphosphate depletion state. CONCLUSIONS: (1) parenteral Fes are highly potent pro-oxidants and capable of inducing tubular and endothelial cell death, (2) markedly different toxicity profiles exist among these agents, and (3) GSH can exert protective effects. However, the latter stems from GSH's glycine content, rather than from a direct antioxidant effect.

Animals↗
PubMed2002

Superoxide anion in Anopheles albimanus hemolymph and midgut is toxic to Plasmodium berghei ookinetes.

The mechanisms of Plasmodium spp. elimination in resistant mosquitoes are not completely understood. Some resistant anopheline strains are able to melanize Plasmodium spp. ookinetes in their midguts. Because quinoid compounds are potent catalysts for free radical generation and because these radicals can be generated in association with melanogenesis, it is probable that they play an important role in the elimination of parasites. The production of the superoxide anion (O-2) in the hemolymph and midgut of Anopheles albimanus female mosquitoes and its cytotoxic effect on Plasmodium berghei ookinetes were analyzed. Ookinetes inoculated into the hemocoel of A. albimanus were covered with melanin and then encapsulated by hemocytes within 1 hr. The presence of O-2 in midguts and in hemolymph obtained by perfusion was verified by the reduction of 3-(4,5 dimethylthiazolil-2)-2,5-diphenyl tetrazolium bromide. O-2 was generated in the hemolymph obtained by perfusion and midguts only in the presence of dihydroxyphenylalanine (L-DOPA), and this reaction was inhibited by superoxide dismutase (SOD). Plasmodium berghei ookinetes exposed to hemolymph plus L-DOPA were killed in vitro, but addition of SOD prevented their killing. Prophenoloxidase transcripts were not observed in midgut epithelium, suggesting that toxic compounds may be imported from the hemolymph. These results suggest that A. albimanus hemolymph and midguts produce O-2 that may limit Plasmodium spp. parasite development.

Animals↗
PubMed1977

H2O2 release from human granulocytes during phagocytosis. Relationship to superoxide anion formation and cellular catabolism of H2O2: studies with normal and cytochalasin B-treated cells.

Normal and cytochalasin B-treated human granulocytes have been studied to determine some of the interrelationships between phagocytosis-induced respiration and superoxide and hydrogen peroxide formation and release into the extracellular medium by intact cells. By using the scopoletin fluorescent assay to continuously monitor extracellular hydrogen peroxide concentrations during contact of cells with opsonized staphylococci, it was demonstrated that the superoxide scavengers ferricytochrome c and nitroblue tetrazolium significantly reduced the amount of H(2)O(2) released with time from normal cells but did not abolish it. This inhibitory effect was reversed by the simultaneous addition of superoxide dismutase (SOD), whereas the addition of SOD alone increased the amount of detectable H(2)O(2) in the medium. The addition of sodium azide markedly inhibited myeloperoxidase-H(2)O(2)-dependent protein iodination and more than doubled H(2)O(2) release, including the residual amount remaining after exposure of the cells to ferricytochrome c, suggesting its origin from an intracellular pool shared by several pathways for H(2)O(2) catabolism. When cells were pretreated with cytochalasin B and opsonized bacteria added, reduced oxygen consumption was observed, but this was in parallel to a reduction in specific binding of organisms to the cells when compared to normal. Under the influence of inhibited phagosome formation by cytochalasin B, the cells released an increased amount of superoxide and peroxide into the extracellular medium relative to oxygen consumption, and all detectable peroxide release could be inhibited by the addition of ferricytochrome c. Decreased H(2)O(2) production in the presence of this compound could not be ascribed to diminished bacterial binding, decreased oxidase activity, or increased H(2)O(2) catabolism and was reversed by the simultaneous addition of SOD. Furthermore, SOD and ferricytochrome c had similar effects on another H(2)O(2)-dependent reaction, protein iodination, in both normal and cytochalasin B cells. When oxygen consumption, O(2.) (-), and H(2)O(2) release were compared in the presence of azide under identical incubation conditions, the molar relationships for normal cells were 1.00:0.34:0.51 and for cytochalasin B-treated cells 1.00:0.99:0.40, respectively. Nonopsonized, or opsonized but disrupted, bacteria did not stimulate any of these metabolic functions. The results indicate that with normal cells approximately 50% of H(2)O(2) released during phagocytosis is derived directly from O(2.) (-) by dismutation, the remainder appearing from an (intra)cellular source shared by azide-inhibitable heme enzymes. With cytochalasin B treatment the evidence is consistent with the derivation of all H(2)O(2) from an O(2.) (-) precursor which is released from the cell surface. Furthermore, when activated by phagocytic particle binding, the neutrophil O(2.) (-) generating system appears to make more of this compound than can be accounted for by dismutation to H(2)O(2). This establishes conditions for the direct participation of both compounds in the microbicidal and cytocidal activity of these cells.

Azides↗
PubMed2003

Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines.

Recently, cannabinoids (CBs) have been shown to possess antitumor properties. Because the psychoactivity of cannabinoid compounds limits their medicinal usage, we undertook the present study to evaluate the in vitro antiproliferative ability of cannabidiol (CBD), a nonpsychoactive cannabinoid compound, on U87 and U373 human glioma cell lines. The addition of CBD to the culture medium led to a dramatic drop of mitochondrial oxidative metabolism [3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H tetrazolium bromide test] and viability in glioma cells, in a concentration-dependent manner that was already evident 24 h after CBD exposure, with an apparent IC(50) of 25 microM. The antiproliferative effect of CBD was partially prevented by the CB2 receptor antagonist N-[(1S)-endo-1,3,3-trimethylbicyclo[2,2,1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; SR2) and alpha-tocopherol. By contrast, the CB1 cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboximide hydrochloride (SR141716; SR1), capsazepine (vanilloid receptor antagonist), the inhibitors of ceramide generation, or pertussis toxin did not counteract CBD effects. We also show, for the first time, that the antiproliferative effect of CBD was correlated to induction of apoptosis, as determined by cytofluorimetric analysis and single-strand DNA staining, which was not reverted by cannabinoid antagonists. Finally, CBD, administered s.c. to nude mice at the dose of 0.5 mg/mouse, significantly inhibited the growth of subcutaneously implanted U87 human glioma cells. In conclusion, the nonpsychoactive CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent.

Animals↗
PubMed2004

Cell survival signalling in heart derived myofibroblasts induced by preconditioning and bradykinin: the role of p38 MAP kinase.

Fibroblasts possess receptors for compounds released during ischemia, including bradykinin. The aims of the present study were to investigate tyrosine kinase and p38 MAP kinase signalling in heart derived myofibroblasts in response to bradykinin and preconditioning ischemia. Fibroblasts from neonatal rat hearts were subjected to pharmacological agents and/or simulated ischemia. Cell viability was measured by the conversion of a tetrazolium salt to its formazan derivative. Preconditioning with 30 min of simulated ischemia followed by 30 min recovery resulted in an 85.4% +/- 7.8% increase in cell survival above that of cells treated with prolonged ischemia alone. Cells treated with bradykinin showed a 35% +/- 7.9 increase in cell survival after lethal ischemia. The B2 receptor antagonist Hoe 140 blocked the protective effect of bradykinin, but did not block preconditioning. The K(ATP) channel blocker glibenclamide and the mitochondria specific K(ATP) blocker 5, hydroxydecanoate, abolished the cytoprotection induced by both preconditioning and bradykinin. The non specific tyrosine kinase inhibitor genistein also abolished the cytoprotection. Effective blockade of cytoprotection was obtained with K(ATP) channel blockers and the tyrosine kinase inhibitor when these compounds were given prior to the preconditioning stimulus and not during the lethal insult. The stress activated protein kinase p38 MAP kinase was investigated by Western blotting and by the use of a specific inhibitor (SB203580). Preconditioning reduced phospho-p38 MAP kinase; in contrast, bradykinin administration markedly increased phosphorylation of p38 MAP kinase. SB203580 protected cells from lethal simulated ischemia. In conclusion, cell survival-signalling pathways activated by bradykinin or simulated ischemia in heart fibroblasts protect via the opening of K(ATP) channels and are independent of the stress-activated p38 MAP kinase and/or related to inhibition of this kinase.

Adrenergic beta-Antagonists↗
PubMed2005

Cytotoxicity of MTA and Portland cement on human ECV 304 endothelial cells.

AIM: To evaluate the cytotoxic effects of two brands of mineral trioxide aggregate (MTA) (Pro-Root MTA and MTA Angelus) and Portland cement (PC) on the human ECV 304 endothelial cell line. METHODOLOGY: Endothelial ECV 304 cells were incubated at 37 degrees C in an atmosphere of 95% air, 5% carbon dioxide and 100% humidity for 7 days and grown in F12 medium supplemented with 10% fetal bovine serum with 50 microg mL(-1) of gentamicin sulphate. Effects of the materials on mitochondrial functions were measured by a colorimetric assay. At each experimental time interval (24, 48 and 72 h), a dimethyl-thiazol-diphenyl tetrazolium bromid assay was conducted to measure cell viability. All assays were repeated three times to ensure reproducibility. Results were expressed as average absorbance (A(570/nm)) +/- SD and the data were analysed statistically by one-way analysis of variance and the Bonferroni post-test. A P-value < 0.05 was considered statistically significant. RESULTS: No statistically significant difference was shown between any of the experimental materials (P > 0.05). CONCLUSIONS: The two brands of MTA analysed, as well as the PC, initially showed a similar elevated cytotoxic effect that decreased gradually with time allowing the cell culture to become reestablished.

Aluminum Compounds↗
PubMed1998

Physiology and tactic response of the phototrophic consortium "Chlorochromatium aggregatum"

The phototrophic consortium "Chlorochromatium aggregatum" was enriched from sediment samples of a eutrophic freshwater lake and was maintained at high numbers in anoxic sulfide-reduced medium. Growth of intact consortia was observed only in the light and in the presence of 2-oxoglutarate as an organic carbon source. Consortia of "C. aggregatum" reached maximum growth rates at light intensities >/= 5 &mgr;mol quanta m-2 s-1. Of ten compounds tested, sulfide, thiosulfate, 2-oxoglutarate, and citrate served as a chemoattractant for "C. aggregatum". When incubated in the presence of sulfide and in the light, epibionts reduced the fluorochrome 5-cyano-2, 3-di-4-tolyl-tetrazolium chloride (CTC). Reduction of CTC was not observed in the presence of the uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) or in the dark, indicating that sulfide serves as an electron donor for the phototrophic epibiont. Motile consortia accumulated scotophobically in microcuvettes at a wavelength of 740 nm. Since this wavelength corresponds to the position of the absorption maximum of bacteriochlorophylls c or d, the photosynthetic pigments are most likely the photoreceptors of the scotophobic response. It is concluded that, within the consortia, a rapid interspecies signal transfer occurs between the nonmotile, green-colored epibiont and the motile, colorless central bacterium.

Journal Article↗
PubMed2002

Development of an injectable, in situ crosslinkable, degradable polymeric carrier for osteogenic cell populations. Part 2. Viability of encapsulated marrow stromal osteoblasts cultured on crosslinking poly(propylene fumarate).

The effect of temporary encapsulation of rat marrow stromal osteoblasts in crosslinked gelatin microparticles on cell viability and proliferation was investigated in this study for microparticles placed on a crosslinking poly(propylene fumarate) (PPF) composite over a 7 day time period. Encapsulated cells were seeded on crosslinking PPF composites at times up to 10 min following initiation of the crosslinking reaction, and also on fully crosslinked PPF composites and tissue culture polystyrene controls, with a cell seeding density of 5.3 x 10(4) cells/cm2. The crosslinked PPF composite exhibited an average gel point of 10.3 min and an average maximum crosslinking temperature of 47.5 degrees C. Cell viability and proliferation were assessed by DNA and 3H-thymidine assays and the results were compared with those for nonencapsulated cells. The results showed that the addition time of cells to a crosslinking PPF composite had a large effect on cell viability and proliferation for both encapsulated and nonencapsulated cells with more surviving cells added at later time points. Most importantly, the temporary encapsulation of cells significantly enhanced cell viability at earlier time points. The data indicate that the presence of gelatin microparticles does not affect the crosslinking of a PPF composite. They further suggest that the temporary encapsulation of cells in crosslinked gelatin microparticles may preserve the viability of cells contained in an actively crosslinking PPF composite used as an injectable polymeric scaffold serving also as a carrier for osteogenic cell populations.

Alkaline Phosphatase↗
PubMed2006

New and simple plate test for screening relative transfructosylation activity of fungi.

Several microorganisms are reported to have transfructosylation activity due to fructosyltransferase and/or fructofuranosidase activities. However, the search for other fungi with higher transfructosylation activity remains a challenge. So, a presumptive and indirect colorimetric plate assay for the evaluation of transfructosylation activity in fungi was developed which involved the simultaneous determination in the same plate of glucose and fructose released from sucrose. The method entailed the (a) glucose oxidase-peroxidase coupled reaction using phenol and 4-aminoantipyrine for determination of glucose; and (b) fructose dehydrogenase oxidation in the presence of a tetrazolium salt for determination of fructose. The presence of enzymes with transfructosylation activity was identified by the formation of pink (presence of glucose) and blue (presence of fructose) halos around the fungal colony. In conclusion, the results showed that the method is suitable for screening a large number of fungi due to its simplicity, reproducibility and rapidity and also gives a relative quantitative idea of the transfructosylation activity of different fungi species.

Ampyrone↗
PubMed1988

Staurosporine, a novel protein kinase inhibitor, enhances HL-60-cell differentiation induced by various compounds.

The effect of staurosporine, a novel calcium/phospholipid-dependent protein kinase (protein kinase C) inhibitor, on differentiation of human promyelocytic leukemic HL-60 cells, was investigated. Staurosporine inhibited HL-60-cell proliferation in a concentration-dependent manner, but did not induce HL-60-cell differentiation by itself. When staurosporine was added to HL-60 cells treated with a suboptimal concentration (1 nM) of 1 alpha,25 dihydroxyvitamin D3 (1,25(OH)2D3), cell differentiation was enhanced in a concentration-dependent manner and the percentages of nitro blue tetrazolium reducing ability and nonspecific esterase activity-positive cells increased from 6% to 51% and from 8% to 54%, respectively, on day 4 at a concentration of 5 nM. Staurosporine (5 nM) achieved almost the same enhancement effect in cultures treated with suboptimal concentrations of 1 nM all-trans-beta-retinoic acid (RA), 3 ng/ml actinomycin D (Act D), 100 microM dibutyryl cyclic adenosine 3':5'-monophosphate (dbc AMP), and 50 microM prostaglandin E1 (PG E1). These results suggest that the inhibition of protein kinase C activity by staurosporine exerts an important role in HL-60-cell differentiation induced by various compounds. Moreover, staurosporine (5 nM) completely inhibited optimal concentrations (50 nM) of [12-o-tetradecanoyl phorbol-13-acetate (TPA)]-induced cell differentiation, but enhanced optimal concentrations of dbc AMP (1 mM)-induced cell differentiation. On the other hand, 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine, which has been reported to inhibit cyclic adenosine 3':5'-monophosphate-dependent protein kinase (protein kinase A) as much as protein kinase C, completely inhibited both cell differentiations induced by optimal concentrations of TPA (50 nM) and induced by optimal concentrations of dbc AMP (1 mM), and did not significantly enhance HL-60-cell differentiation induced by suboptimal concentrations of 1,25(OH)2D3, RA, and dbc AMP. Therefore, these results suggest that the inhibition of protein kinase C, which is not accompanied by that of protein kinase A, is concerned with the induction of HL-60-cell differentiation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMedDate not supplied

Growth inhibition and induction of differentiation and apoptosis mediated by sodium butyrate in Caco-2 cells with algal glycolipids.

Glycolipids should have potential effects as antitumor agents. However, very few studies have examined this property of digalactosyl diacylglycerol (DGDG) and sulfoquinovosyl diacylglycerol (SQDG) on colon cancer cells. Cell viability was determined every 24 h with sodium 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2, 4-disulfophenyl)-2H-tetrazolium dye reduction assay up to 72 h. Alkaline phosphatase activity was measured for assessing cell differentiation. Apoptosis was tested with enzyme-linked immunosorbent assay analysis. Growth of Caco-2 cells was inhibited apparently at 48 h after addition of SQDG and at 72 h with DGDG. Alkaline phosphatase activity of Caco-2 cells obviously increased in combination with DGDG or SQDG and sodium butyrate (NaBT) at 72 h, indicating that DGDG and SQDG enhanced cell differentiation induced with NaBT. An increased enrichment factor was found when the cell was treated in combination with DGDG or SQDG and NaBT. These results strongly suggest that DGDG and SQDG should be considered as the leading compounds of potentially useful colon cancer chemotherapy agents when NaBT is combined.

Alkaline Phosphatase↗
PubMed2003

Reduction mechanism of tetrazolium salt XTT by a glucosamine derivative.

XTT (3'-[1-[(phenylamino)-carbonyl]-3,4-tetrazolium]-bis(methoxy-6-nitro)benzenesulfonic acid hydrate) was reduced by incubated glucosamine hydrochloride. The XTT reducibility by incubated glucosamine was linearly related with the DNA-breaking activity. In order to elucidate the reaction mechanism, the glucosamine derivatives formed during the incubation process were separated by HPLC, and the compound responsible for the reduction was analyzed. Among the incubated products, fructosazine and deoxyfructosazine were identified by LC-MS, FAB-MS, and 1H- and 13C-NMR. These products showed no XTT reducibility, but an unstable intermediate with a molecular weight of 322 displayed reducibility. Since the intermediate gave fructosazine by oxidation with XTT and was a precursor of deoxyfructosazine, we conclude that the intermediate could have been dihydrofructosazine. Therefore, the XTT reducibility by incubated glucosamine was based on dihydrofructosazine formed by the condensation of two molecules of glucosamine.

Chromatography, High Pressure Liquid↗
PubMed2004

Integrated assessment for anaerobic biodegradability of organic compounds using the analytical hierarchy process.

Anaerobic biodegradability of organic compounds can be assessed from the changes in organic compounds, the end products, and the activity of microorganisms. In this study, all three of these variables were considered to integrate assessment of the anaerobic biodegradability of organic compounds. The analytical hierarchy process (AHP) was introduced to integrate the assessment. Real values between 0 and 10 were determined in the pairwise comparison matrix according to the values of assessment indices of the three variables. A new adjustment method, which can obtain minimum adjustment of the values in matrix, was proposed to reach the acceptable consistency of the matrix. Finally, the anaerobic biodegradability of 14 organic compounds was assessed using AHP.

Anaerobiosis↗
PubMed2005

Rationale for using Peltophorum africanum (Fabaceae) extracts in veterinary medicine.

Peltophorum africanum (Fabaceae) is a deciduous tree widespread in southern Africa. The plant has many ethnomedical and ethnoveterinary uses. Root and bark decoctions are used to treat diarrhoea, dysentery, sore throat, wounds, back and joint pains, HIV-AIDS, venereal diseases and infertility. Pastoralists and rural farmers use the root and bark extracts to treat diarrhoea, dysentery, infertility, and to promote well-being and resistance to diseases in cattle. To evaluate these ethnobotanical leads, dried leaves, stem bark and root bark were extracted with ethanol, acetone, dichloromethane and hexane. Polyphenols in the extract were determined by the Folin-Ciocalteu method with gallic acid as standard. Qualitative antioxidant activity was screened by spraying thin layer chromatograms (TLC) of the extracts with 0.2% 1,1-diphenyl-2-picryl hydrazyl (DPPH), and quantified with Trolox equivalent antioxidant capacity (TEAC) assay. Minimum inhibitory concentration (MIC) and total antibacterial activity (TAA) were determined by serial microplate dilution for Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa and Enterococcus faecalis, with gentamicin as standard and tetrazolium violet as growth indicator. Acetone and ethanol extracted the largest quantity of material. Polyphenols concentration was 49.2% in acetone extract of the root and 3.8% in dichloromethane extract of the leaf. Antioxidant activity of at least 5 antioxidant compounds as measured by TEAC ranged from 1.34 (ethanol extract of the root) to 0.01 (hexane extract of the leaf). The total antibacterial activity (volume to which active compounds present in 1 g plant material can be diluted and still inhibit bacterial growth) was 1263 ml/g for ethanol extract of the root against S. aureus, and 800 ml/g for acetone extract of the root against P. aeruginosa. There was substantial activity against both Gram-positive and Gram-negative bacteria, with MIC values of 0.08 mg/ml for S. aureus and 0.16 mg/ml for P. aeruginosa. There is therefore a rationale for the traditional use of root and bark of P. africanum in treating bacterial infection related diseases.

Animals↗