Nephrotoxicity of cisplatin (CP) involves renal oxidative stress and inflammation, and sesamin (a major liganin in many plants) has strong antioxidant and antiinflammatory actions. Therefore, we investigated here the possible mitigative action of sesamin on CP nephrotoxicity in rats. Sesamin was given orally (5 mg/kg/day, 10 days), and on the 7th day, some of the treated rats were injected intraperitoneally with either saline or CP (5 mg/kg). On the 11th day, rats were sacrificed, and blood and urine samples and kidneys were collected for biochemical estimation of several traditional and novel indices of renal damage in plasma and urine, several oxidative and nitrosative indices in kidneys, and assessment of histopathological renal damage. CP significantly and adversely altered all the physiological, biochemical and histopathological indices of renal function measured. Kidneys of CP-treated rats had a moderate degree of necrosis. This was markedly lessened when CP was given simultaneously with sesamin. Sesamin treatment did not significantly alter the renal CP concentration. The results suggested that sesamin had ameliorated CP nephrotoxicity in rats by reversing the CP-induced oxidative stress and inflammation. Pending further pharmacological and toxicological studies sesamin may be considered a potentially useful nephroprotective agent.

• MeSH
• antioxidancia farmakologie   terapeutické užití   MeSH
• antitumorózní látky škodlivé účinky   MeSH
• cisplatina škodlivé účinky   MeSH
• dioxoly farmakologie   terapeutické užití   MeSH
• fytoterapie * MeSH
• ledviny účinky léků   metabolismus   MeSH
• lignany farmakologie   terapeutické užití   MeSH
• nemoci ledvin chemicky indukované   farmakoterapie   metabolismus   MeSH
• potkani Wistar MeSH
• preklinické hodnocení léčiv MeSH
• rostlinné extrakty terapeutické užití   MeSH
• Sesamum * MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antioxidancia MeSH
• antitumorózní látky MeSH
• cisplatina MeSH
• dioxoly MeSH
• lignany MeSH
• rostlinné extrakty MeSH
• sesamin MeSH Prohlížeč

Warfarin is a commonly used anticoagulant drug and is a derivate of coumarin. Cytochrome P450 2C9 (CYP2C9) plays the key role in transformation of coumarin and thus, influences determination of warfarin dosage. A number of factors including dietary compounds such as sesamin, caffeic acid and ferulic acids can regulate the activity of CYP2C9. The present study tested the hypothesis that sesamin, episesamin, caffeic acid and ferulic acid decreases the rate of warfarin 7-hydroxylation via inhibition of hepatic CYP2C9. The experiments were conducted on hepatic microsomes from human donors. It was demonstrated that the rate of 7-hydroxylation of warfarin was significantly decreased in the presence of sesamin in the range of concentrations from 5 to 500 nM, and was not affected by episesamin, caffeic acid and ferulic acid in the same range of concentrations. The kinetic analysis indicated non-competitive type of inhibition by sesamin with Ki = 202 ± 18 nM. In conclusion, the results of our in vitro study revealed that sesamin was able to inhibit formation of a major metabolite of warfarin, 7-hydroxywarfarin. The potentially negative consequences of the consumption of high amounts of sesamin-containing food or dietary supplements in warfarin-treated patients need to be further studied.

• Klíčová slova
• Cytochrome P450, Detoxification, Food-drug interactions, In vitro, S-7-hydroxywarfarin,
• MeSH
• antikoagulancia metabolismus   MeSH
• dioxoly chemie   farmakologie   MeSH
• hydroxylace MeSH
• inhibiční koncentrace 50 MeSH
• jaterní mikrozomy metabolismus   MeSH
• kinetika MeSH
• kyseliny kávové farmakologie   MeSH
• kyseliny kumarové farmakologie   MeSH
• lidé MeSH
• lignany chemie   farmakologie   MeSH
• potraviny MeSH
• potravní doplňky MeSH
• warfarin metabolismus   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antikoagulancia MeSH
• caffeic acid MeSH Prohlížeč
• dioxoly MeSH
• ferulic acid MeSH Prohlížeč
• kyseliny kávové MeSH
• kyseliny kumarové MeSH
• lignany MeSH
• sesamin MeSH Prohlížeč
• warfarin MeSH

The aim of the present study was to evaluate in vitro effects of dietary phytochemicals naringenin, quercetin, and sesamin on the activities of ethoxy- (EROD; CYP1A) and benzyloxy- (BROD; CYP3A) resorufin O-dealkylases after the exposure to the cocktail of persistent organic pollutants (POPs). CD-1 mice were exposed from weaning, through gestation and lactation to a defined mixture of POPs. Hepatic microsomes were prepared from their female offspring at postnatal day 42. Hepatic EROD and BROD activity were evaluated in the presence of quercetin, naringenin, and sesamin at nine concentrations from 5 to 100000 nM. EROD activity was strongly inhibited by quercetin with Ki values from 1.7 to 2.6 μM. BROD activity was inhibited by quercetin with Ki values from 64.9 to 75.3 μM and naringenin with Ki values from 39.3 to 45.8 μM. The IC50 and Ki values did not differ between the groups of mice with different levels of POPs exposure in any of the experimental sets. Sesamin did not inhibit either EROD or BROD. We concluded that the interactions of quercetin and naringenin with CYP1A and CYP3A in mice liver were not affected by the levels of POPs exposure.

• MeSH
• cytochrom P-450 CYP3A MeSH
• dioxoly farmakologie   MeSH
• flavanony farmakologie   MeSH
• jaterní mikrozomy enzymologie   patologie   MeSH
• látky znečišťující vzduch toxicita   MeSH
• lignany farmakologie   MeSH
• matka - expozice noxám škodlivé účinky   MeSH
• myši MeSH
• quercetin farmakologie   MeSH
• rodina 1 cytochromu P450 metabolismus   MeSH
• systém (enzymů) cytochromů P-450 metabolismus   MeSH
• těhotenství MeSH
• zpožděný efekt prenatální expozice chemicky indukované   enzymologie   patologie   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• CYP3A protein, mouse MeSH Prohlížeč
• cytochrom P-450 CYP3A MeSH
• dioxoly MeSH
• flavanony MeSH
• látky znečišťující vzduch MeSH
• lignany MeSH
• naringenin MeSH Prohlížeč
• quercetin MeSH
• rodina 1 cytochromu P450 MeSH
• sesamin MeSH Prohlížeč
• systém (enzymů) cytochromů P-450 MeSH

The effect of beta(3)-adrenoceptor (beta(3)-AR) agonists on adipocytes treated or not treated with signaling modulators has not been sufficiently elucidated. Using rat epididymal adipocytes (adipocytes) labeled with [(32)P]orthophosphate, we found that treatment with the selective beta(3)-AR agonist CL316243 (CL; 1 microM) induces phosphatidylinositol (PI) 3,4,5-triphosphate (PI[3,4,5]P(3)) production and that this response is inhibited by adenosine deaminase (ADA, an adenosine-degrading enzyme; 2 U/ml), pertussis toxin (PTX, an inactivator of inhibitory guanine-nucleotide-binding protein; 1 microg/ml), or wortmannin (WT, a PI-kinase inhibitor; 3 microM). The results showed that CL induced PI(3,4,5)P(3) production in intact adipocytes and that this production was affected by signaling modulators. Taken together, our findings indicate that CL produces PI(3,4,5)P(3) in an ADA-sensitive, PTX-sensitive, or WT-sensitive manner and will advance understanding of the effect of beta(3)-AR agonists on adipocytes.

• MeSH
• adenosindeaminasa MeSH
• agonisté beta-3-adrenergních receptorů farmakologie   MeSH
• androstadieny MeSH
• dioxoly farmakologie   MeSH
• fosfatidylinositolfosfáty metabolismus   MeSH
• krysa rodu Rattus MeSH
• pertusový toxin MeSH
• tukové buňky účinky léků   enzymologie   MeSH
• wortmannin MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• adenosindeaminasa MeSH
• agonisté beta-3-adrenergních receptorů MeSH
• androstadieny MeSH
• dioxoly MeSH
• disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate MeSH Prohlížeč
• fosfatidylinositolfosfáty MeSH
• pertusový toxin MeSH
• phosphatidylinositol 3,4,5-triphosphate MeSH Prohlížeč
• wortmannin MeSH

The tetrahydroisoquinoline trabectedin is a marine compound with approved activity against human soft-tissue sarcoma. It exerts antiproliferative activity mainly by specific binding to the DNA and inducing DNA double-strand breaks (DSB). As homologous recombination repair (HRR)-deficient tumors are more susceptible to trabectedin, hyperthermia-mediated on-demand induction of HRR deficiency represents a novel and promising strategy to boost trabectedin treatment. For the first time, we demonstrate enhancement of trabectedin effectiveness in human sarcoma cell lines by heat and characterize cellular events and molecular mechanisms related to heat-induced effects. Hyperthermic temperatures (41.8 or 43°C) enhanced significantly trabectedin-related clonogenic cell death and G2/M cell cycle arrest followed by cell type-dependent induction of apoptosis or senescence. Heat combination increased accumulation of γH2AX foci as key marker of DSBs. Expression of BRCA2 protein, an integral protein of the HRR machinery, was significantly decreased by heat. Consequently, recruitment of downstream RAD51 to γH2AX-positive repair foci was almost abolished indicating relevant impairment of HRR by heat. Accordingly, enhancement of trabectedin effectiveness was significantly augmented in BRCA2-proficient cells by hyperthermia and alleviated in BRCA2 knockout or siRNA-transfected BRCA2 knockdown cells. In peripheral blood mononuclear cells isolated from sarcoma patients, increased numbers of nuclear γH2AX foci were detected after systemic treatment with trabectedin and hyperthermia of the tumor region. The findings establish BRCA2 degradation by heat as a key factor for a novel treatment strategy that allows targeted chemosensitization to trabectedin and other DNA damaging antitumor drugs by on-demand induction of HRR deficiency.

• Klíčová slova
• DNA repair, hyperthermia, sarcoma, trabectedin,
• MeSH
• antitumorózní látky alkylující farmakologie   MeSH
• apoptóza účinky léků   účinky záření   MeSH
• biologické modely MeSH
• chemorezistence účinky záření   MeSH
• dioxoly farmakologie   MeSH
• histony metabolismus   MeSH
• indukovaná hypertermie * MeSH
• kaspasy metabolismus   MeSH
• kontrolní body buněčného cyklu účinky léků   účinky záření   MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• protein BRCA2 metabolismus   MeSH
• proteolýza účinky léků   účinky záření   MeSH
• rekombinační oprava DNA účinky léků   účinky záření   MeSH
• rekombinasa Rad51 metabolismus   MeSH
• sarkom metabolismus   patologie   terapie   MeSH
• tetrahydroisochinoliny farmakologie   MeSH
• trabektedin MeSH
• transport proteinů MeSH
• vazba proteinů MeSH
• viabilita buněk účinky léků   účinky záření   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antitumorózní látky alkylující MeSH
• dioxoly MeSH
• histony MeSH
• kaspasy MeSH
• protein BRCA2 MeSH
• rekombinasa Rad51 MeSH
• tetrahydroisochinoliny MeSH
• trabektedin MeSH

1. This study examined hepatic cytochrome P450 (CYP450) response to dietary sesamin in combination with different n-6/n-3 fatty acid ratios in fish diet. Over a period of 4 months, fish were fed seven different experimental diets an n-6/n-3 FA ratio of either 0.5 or 1.0 in combination with two sesamin levels: low sesamin = 1.16 g/kg feed and high sesamin = 5.8 g/kg feed. Control diets did not contain sesamin. 2. The CYP450-associated activities of ethoxyresorufin O-deethylase (EROD), 7-benzyloxy-4-trifluoromethylcoumarin O-debenzylation (BFCOD), pentoxyresorufin O-depentylase (PROD), coumarin hydroxylase (COH), methoxyresorufin O-deethylase (MROD) and p-nitrophenol hydroxylase (PNPH) were significantly induced by dietary sesamin in a dose-related manner. 3. Expressions of the genes CYP1A1, CYP1A3, CYP3A, AhR1α, AhR2β, AhR2δ and PXR involved in the regulation of CYP450 activities, was not the primary source of this induction.

• Klíčová slova
• Fish, induction, xenobiotic metabolizing enzymes,
• MeSH
• dioxoly farmakologie   MeSH
• játra účinky léků   enzymologie   MeSH
• lignany farmakologie   MeSH
• oleje rostlin farmakologie   MeSH
• regulace genové exprese účinky léků   MeSH
• rybí oleje farmakologie   MeSH
• Salmo salar metabolismus   MeSH
• systém (enzymů) cytochromů P-450 metabolismus   MeSH
• xenobiotika metabolismus   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• dioxoly MeSH
• lignany MeSH
• oleje rostlin MeSH
• rybí oleje MeSH
• sesamin MeSH Prohlížeč
• systém (enzymů) cytochromů P-450 MeSH
• xenobiotika MeSH

Responses of adipose cells to adrenoceptor regulation, including that of β-adrenoceptor (AR), and the signalling machinery involved in these responses are not sufficiently understood; information that is helpful for elucidating the adrenoceptor (adrenergic and β-AR)-responsive machinery is insufficient. We examined phospho-Thr-172 AMPK production in mouse-derived 3T3-L1 adipocytes treated with epinephrine or CL316243 (a β3-AR agonist) for 15 min. We also examined MAPK activation or G protein-associated PI3K activation or -associated PI3K p85 complex formation in rat epididymal (white) adipocytes treated with CL316243 for 15 min or aluminum fluoride (a G-protein signalling activator) for 20 min. Furthermore, we examined the effect of PTX (a trimeric G-protein inactivator) on p85 complex formation induced by aluminum fluoride treatment. Western blot analysis revealed that epinephrine or CL316243 treatment increased the phospho- Thr-172 AMPK (an active form of AMPK) level in 3T3-L1 adipocytes. Activated kinase analysis with a specific substrate showed that CL316243 or aluminum fluoride treatment activated MAPK in rat adipocytes. Immunoprecipitation experiments with a G-protein β subunit (Gβ) antibody showed that treatment of rat adipocytes with CL316243 activated PI3K and increased the PI3K p85 level in the Gβ antibody immunoprecipitates. Such an increase in the p85 level was similarly elicited by aluminum fluoride treatment in a PTX-sensitive manner. Our results provide possible clues for clarifying the signalling machinery involved in adrenoceptor responses, including those of β3-AR, in mouse-derived adipocytes and rat white adipocytes. Our findings advance the understanding of responses to adrenoceptor regulation in adipose cells and of the cellular signalling machinery present in the cells.

• MeSH
• adrenalin farmakologie   MeSH
• bílé tukové buňky enzymologie   MeSH
• buňky 3T3-L1 MeSH
• dioxoly farmakologie   MeSH
• fluoridy farmakologie   MeSH
• fosfatidylinositol-3-kinasy metabolismus   MeSH
• fosfothreonin metabolismus   MeSH
• imunoprecipitace MeSH
• krysa rodu Rattus MeSH
• mitogenem aktivované proteinkinasy metabolismus   MeSH
• myši MeSH
• pertusový toxin farmakologie   MeSH
• proteinkinasy aktivované AMP metabolismus   MeSH
• proteiny vázající GTP metabolismus   MeSH
• sloučeniny hliníku farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• adrenalin MeSH
• aluminum fluoride MeSH Prohlížeč
• dioxoly MeSH
• disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate MeSH Prohlížeč
• fluoridy MeSH
• fosfatidylinositol-3-kinasy MeSH
• fosfothreonin MeSH
• mitogenem aktivované proteinkinasy MeSH
• pertusový toxin MeSH
• proteinkinasy aktivované AMP MeSH
• proteiny vázající GTP MeSH
• sloučeniny hliníku MeSH

During embryogenesis, the Activin/Nodal pathway promotes the mesendodermal lineage and inhibits neural fate. The molecular mechanisms underlying this role of the Activin/Nodal pathway are not clear. In this study, we report a role for protein tyrosine phosphatase 1B (PTP1B) in Activin-mediated early fate decisions during ESC differentiation and show that PTP1B acts as an effector of the Activin pathway to specify mesendodermal or neural fate. We found that the Activin/ALK4 pathway directly recruits PTP1B and stimulates its release from the endoplasmic reticulum through ALK4-mediated cleavage. Subsequently, PTP1B suppresses p-ERK1/2 signaling to inhibit neural specification and promote mesendodermal commitment. These findings suggest that a noncanonical Activin signaling pathway functions in lineage specification of mouse and human embryonic stem cells.

• MeSH
• aktivinové receptory typu I chemie   metabolismus   MeSH
• aktiviny metabolismus   MeSH
• benzamidy farmakologie   MeSH
• buněčná diferenciace * účinky léků   MeSH
• buněčný rodokmen účinky léků   MeSH
• dioxoly farmakologie   MeSH
• embryonální kmenové buňky cytologie   účinky léků   enzymologie   MeSH
• endoderm cytologie   účinky léků   metabolismus   MeSH
• extracelulárním signálem regulované MAP kinasy metabolismus   MeSH
• fosforylace účinky léků   MeSH
• lidé MeSH
• MAP kinasový signální systém účinky léků   MeSH
• mezoderm cytologie   účinky léků   metabolismus   MeSH
• molekulární sekvence - údaje MeSH
• myši MeSH
• neurony cytologie   účinky léků   metabolismus   MeSH
• pluripotentní kmenové buňky cytologie   účinky léků   metabolismus   MeSH
• protein Smad2 metabolismus   MeSH
• sekvence aminokyselin MeSH
• signální transdukce * účinky léků   MeSH
• tyrosinfosfatasa nereceptorového typu 1 metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide MeSH Prohlížeč
• ACVR1B protein, human MeSH Prohlížeč
• Acvr1b protein, mouse MeSH Prohlížeč
• aktivinové receptory typu I MeSH
• aktiviny MeSH
• benzamidy MeSH
• dioxoly MeSH
• extracelulárním signálem regulované MAP kinasy MeSH
• protein Smad2 MeSH
• tyrosinfosfatasa nereceptorového typu 1 MeSH

Several lines of evidence suggest that in mice the activation of SMAD2/3 signaling by oocyte secreted factors, together with epidermal growth factor receptor (EGFR) activation, is essential to induce cumulus expansion. Here we show that inhibition of EGFR kinase in follicle stimulating hormone (FSH)-stimulated porcine oocyte-cumulus cell complex (OCCs) strongly decreases hyaluronan (HA) synthesis and its retention in the matrix, as well as progesterone synthesis. Although porcine cumulus cells undergo expansion independently of oocytes, we use biochemical and gene expression analyses to show that they do require activation of SMAD2/3 for optimal stimulation of HA synthesis and proteins involved in the organization of this polymer in the expanded matrix. Furthermore, FSH-induced progesterone synthesis by porcine cumulus cells was increased by blocking SMAD2/3 activation. In conclusion, these results support the hypothesis that an FSH-EGF autocrine loop is active in porcine OCCs, and provide the first evidence that the SMAD2/3 signaling pathway is induced by paracrine/autocrine factors in porcine cumulus cells and is involved in the control of both cumulus expansion and steroidogenesis.

• MeSH
• benzamidy farmakologie   MeSH
• C-reaktivní protein metabolismus   MeSH
• chinazoliny farmakologie   MeSH
• dioxoly farmakologie   MeSH
• epidermální růstový faktor metabolismus   MeSH
• erbB receptory antagonisté a inhibitory   metabolismus   MeSH
• folikuly stimulující hormon metabolismus   MeSH
• glukuronosyltransferasa antagonisté a inhibitory   metabolismus   MeSH
• isochinoliny farmakologie   MeSH
• kumulární buňky metabolismus   MeSH
• kyselina hyaluronová biosyntéza   MeSH
• meióza účinky léků   MeSH
• molekuly buněčné adheze antagonisté a inhibitory   metabolismus   MeSH
• myši MeSH
• oocyty enzymologie   fyziologie   MeSH
• prasata MeSH
• progesteron biosyntéza   MeSH
• protein Smad2 antagonisté a inhibitory   metabolismus   MeSH
• protein Smad3 antagonisté a inhibitory   metabolismus   MeSH
• pyridiny farmakologie   MeSH
• pyrroly farmakologie   MeSH
• sérový amyloidový protein metabolismus   MeSH
• signální transdukce účinky léků   MeSH
• tyrphostiny farmakologie   MeSH
• vývojová regulace genové exprese účinky léků   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide MeSH Prohlížeč
• 6,7-dimethyl-2-(2E)-3-(1-methyl-2-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl-prop-2-enoyl)-1,2,3,4-tetrahydroisoquinoline hydrochloride MeSH Prohlížeč
• benzamidy MeSH
• C-reaktivní protein MeSH
• chinazoliny MeSH
• dioxoly MeSH
• epidermální růstový faktor MeSH
• erbB receptory MeSH
• folikuly stimulující hormon MeSH
• glukuronosyltransferasa MeSH
• isochinoliny MeSH
• kyselina hyaluronová MeSH
• molekuly buněčné adheze MeSH
• progesteron MeSH
• protein Smad2 MeSH
• protein Smad3 MeSH
• PTX3 protein MeSH Prohlížeč
• pyridiny MeSH
• pyrroly MeSH
• RTKI cpd MeSH Prohlížeč
• sérový amyloidový protein MeSH
• tyrphostiny MeSH

Based on our previous studies, 21 new halogenated 3-(4-alkylphenyl)-1,3-benzoxazine-2,4-(3H)-diones were synthesized by the reaction of salicylanilides and methyl-chloroformate. All compounds were screened in vitro against three different strains of mycobacterium, and Free-Wilson method was used to establish structure-activity relationships. 6-Bromo-3-(4-butylphenyl)-1,3-benzoxazine-2,4-(3H)-dione 3b proved to be the most active compound of the series.

• MeSH
• antituberkulotika chemická syntéza   chemie   farmakologie   MeSH
• dioxoly izolace a purifikace   farmakologie   MeSH
• fenoly izolace a purifikace   farmakologie   MeSH
• magnetická rezonanční spektroskopie MeSH
• mikrobiální testy citlivosti MeSH
• Mycobacterium účinky léků   MeSH
• oxaziny chemická syntéza   chemie   farmakologie   MeSH
• salicylanilidy chemická syntéza   chemie   farmakologie   MeSH
• vztahy mezi strukturou a aktivitou MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 3-(2-(7-methoxybenzo(d)(1,3)dioxol-5-yl)ethyl)phenol MeSH Prohlížeč
• 6-(3-hydroxyphenethyl)benzo(d)(1,3)dioxol-4-ol MeSH Prohlížeč
• antituberkulotika MeSH
• dioxoly MeSH
• fenoly MeSH
• oxaziny MeSH
• salicylanilidy MeSH