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PubMedDate not supplied

Effect of 7,8-benzoflavone pretreatment on diethylstilbestrol metabolism, drug-metabolising enzymes and the aromatic hydrocarbon (Ah) receptor in male hamster liver.

Pretreatment of male Syrian golden hamsters with 7,8-benzoflavone (7,8-BF) leads to a marked increase of cytochrome P450 and cytochrome b5 levels in the liver, whereas phenobarbital (PB) and 3-methylcholanthrene (MC) induce cytochrome P450 but not cytochrome b5 7,8-BF pretreatment has only minor effects on the activities of aryl hydrocarbon hydroxylase and 7-ethoxycoumarin-O-deethylase, but 7-ethoxyresorufin-O-deethylase is increased 3-fold. In contrast to PB, pretreatment with 7,8-BF or MC reduces the oxidative metabolism of diethylstilbestrol (DES) by hepatic microsomes in vitro. The cytosolic level of the aromatic hydrocarbon (Ah) receptor in hamster liver is decreased by 7,8-BF and slightly enhanced by MC pretreatment. PB increases the receptor level 1.5-fold. The affinity of 7,8-BF to the Ah receptor in vitro is of the same order of magnitude as that of the known ligands 5,6-benzoflavone and 2,3,7,8-tetrachlorodibenzofurane. PB and DES show no binding to the receptor protein.

Animals↗
PubMed2003

7,8-Benzoflavone: a phytotoxin from root exudates of invasive Russian knapweed.

Root exudates from Acroptilon repens (Russian knapweed) were found to be phytotoxic and the phytotoxin in the exudate was identified as 7,8-benzoflavone (alpha-naphthoflavone), (1), not previously known as a natural product. In tests on growing seedlings both 1 and its isomer 5,6-benzoflavone (2) were phytotoxic. Flavone, a structural analog of 1 and a known granular leaf and stem exudate of other plant species, was also phytotoxic and more potent than 1 or 2.

Arabidopsis↗
PubMed1988

Alteration of methylcholanthrene-mediated suppression of cutaneous delayed hypersensitivity by benzoflavone treatment of C57BL/6J mice.

The potential role of the cytochromes P-450 in methylcholanthrene (MC)-mediated suppression of cutaneous delayed hypersensitivity (CDH) in C57BL/6J (B6) mice was evaluated indirectly by treating mice with agents known to induce or inhibit hepatic cytochromes P-450 prior to contact sensitization. Subsequent alterations in aryl hydrocarbon hydroxylase (AHH) activity and CDH, as measured by suppression of 2,4-dinitrofluorobenzene (DNFB)-induced ear swelling, were measured. MC administration resulted in a dose-dependent suppression of ear swelling and a concomitant dose-dependent induction of hepatic AHH activity. Treatment of B6 mice with phenobarbital (PB), 80 mg/kg daily X 3, a broad spectrum inducer of P-450, resulted in a 2.5-fold increase in benzo[a]pyrene (B[a]P) hydroxylase activity without affecting CDH. Animals treated with the same PB protocol prior to an ED20 dose of MC showed no difference in suppression of CDH compared to animals treated with MC alone. In contrast, successive treatment with the selective P1-450 inducer, 5,6-benzoflavone (beta NF), prior to and following an ED20 dose of MC significantly increased suppression of CDH (p less than 0.001) usually seen at this MC dose. Treatment with a known inhibitor of cytochrome P1-450 activity, 7,8-benzoflavone (alpha NF), did not prevent AHH induction when administered prior to and following MC (ED100) nor did it suppress CDH when administered alone. However, this alpha NF treatment completely prevented suppression of CDH usually seen at this MC dose. These data provide evidence suggesting that metabolic activation by cytochrome P1-450 is required for the expression of the immunosuppressive activity of MC.

Animals↗
PubMed2003

Drug/substance reversal effects of a novel tri-substituted benzoflavone moiety (BZF) isolated from Passiflora incarnata Linn.--a brief perspective.

The present work is a mini-review of the author's original work on the plant Passiflora incarnata Linn., which is used in several parts of the world as a traditional medicine for the management of anxiety, insomnia, epilepsy and morphine addiction. A tri-substituted benzoflavone moiety (BZF) has been isolated from the bioactive methanol extract of this plant, which has been proposed in the author's earlier work to be responsible for the biological activities of this plant. The BZF moiety has exhibited significantly encouraging results in the reversal of tolerance and dependence of several addiction-prone psychotropic drugs, including morphine, nicotine, ethanol, diazepam and delta-9-tetrahydrocannabinol, during earlier pharmacological studies conducted by the author. In addition to this, the BZF moiety has exhibited aphrodisiac, libido-enhancing and virility-enhancing properties in 2-year-old male rats. When administered concomitantly with nicotine, ethanol and delta-9-tetrahydrocannabinol for 30 days in male rats, the BZF also prevented the drug-induced decline in sexuality in male rats. Because the BZF moiety isolated from P. incarnata is a tri-substituted derivative of alpha-naphthoflavone (7,8-benzoflavone), a well-known aromatase-enzyme inhibitor, the mode of action of BZF has been postulated to be a neurosteroidal mechanism vide in which the BZF moiety prevents the metabolic degradation of testosterone and upregulates blood - testosterone levels in the body. As several flavonoids (e.g. chrysin, apigenin) and other phytoconstituents also possess aromatase-inhibiting properties, and the IC50 value of such phytomoieties is the main factor determining their biochemical efficacy, by altering their chemical structures to attain a desirable IC50 value new insights in medical therapeutics can be attained, keeping in view the menace of drug abuse worldwide.

Animals↗
PubMed1979

Effect of trichloropropene oxide and benzoflavone on polycyclic hydrocarbon carcinogenesis in C3H/He and DBA/2 mice.

Effect of 1,1,1-trichloropropene 2,3-oxide and 7,8-benzoflavone on benzo[a]-pyrene and 3-methylcholanthrene carcinogenesis in the subcutaneous tissues of C3H/He and DBA/2 mice was examined. By a single application of the carcinogen, the incidence of fibrosarcoma was higher and the latency of tumorigenesis was shorter in C3H/He mice than in DBA/2 mice. Treatment with 1,1,1-trichloropropene 2,3-oxide increased the incidence of fibrosarcoma in DBA/2 mice, but decreased the rate in C3H/He mice, when benzo[a]pyrene was used as a carcinogen. On the other hand, in 3-methylcholanthrene carcinogenesis, no effect of the oxide on the tumor incidence was observed. By the simultaneous application of 7,8-benzoflavone with benzo[a]pyrene, the tumor incidence increased, but not so significantly in DBA/2 mice, compared to that treated with benzo[a]pyrene alone, and no appreciable effect was observed in C3H/He mice treated with benzo[a]pyrene, and in both strains of mice with 3-methylcholanthrene. The relationship between the activity of arylhydrocarbon hydroxylase and the change in polycyclic hydrocarbon carcinogenesis is briefly discussed.

Animals↗
PubMed1979

Inducibility of microsomal enzymes in normal and pre-cancerous lung tissue. Synergistic action of 5-6 benzoflavon or methyl-cholanthrene in radiation induced carcinogenesis.

The inducibility of pulmonary microsomal enzymes and the biological effects of chronic induction by 5-6 benzoflavone and methylcholanthrene were compared in normal and precancerous rats. Two important points were shown out: a dose of 6000 WLM resulted in a permanent modification of the pulmonary microsomal enzymatic pool and 5-6 benzoflavon was a strong co-factor of radiation induced carcinogenesis. This synergistic action was demonstrated by a much shorter latency, moreover neo-formed tissue and epidermoid cancers with a particular morphology were observed. In all the cases cancers appeared within 100 days following the beginning of the chemical treatment.

Animals↗
PubMed1970

Dimethylbenzanthracene tumorigenesis and aryl hydrocarbon hydroxylase in mouse skin: inhibition by 7,8-benzoflavone.

Mouse skin contains aryl hydrocarbon hydroxylase which is highly inducible. The enzyme system is inhibited when 7,8-benzoflavone is added to homogenates of skin epidermis. 7,8-Benzoflavone also inhibits mouse skin tumorigenesis caused by repeated treatment with 9,10-dimethylbenzanthracene or by a single treatment with this chemical followed by weekly treatment with croton oil. These findings suggest that this enzyme system may be responsible for the activation of 9,10-dimethylbenzanthracene to its carcinogenic form.

Animals↗
PubMed1988

Effect of pretreatment with 7,8-benzoflavone and diethylstilbestrol on the hepatic metabolism of diethylstilbestrol in the male Syrian golden hamster in vivo.

Liver tumors are induced in male Syrian golden hamsters by the combined treatment with diethylstilbestrol (DES) and 7,8-benzoflavone (7,8-BF), but not with either substance alone. With the aim of clarifying whether metabolic activation of DES is involved in the mechanism of tumorigenesis in this animal model, we have studied the effect of pretreatment with 7,8-BF alone, DES alone, and 7,8-BF plus DES for 2, 8, 20 and 32 weeks on the hepatic in vivo metabolism of DES, using biliary metabolites collected from bile-duct cannulated male hamsters as probe. Formation of glucuronides and sulfates was not affected by treatment with 7,8-BF nor 7,8-BF plus DES. In contrast, animals pretreated with DES alone had a decreased amount of glucuronides and an increased proportion of unconjugated material in the bile. Oxidative metabolism of DES was not significantly altered in hamsters treated with 7,8-BF for up to 20 weeks, whereas pretreatment with DES alone and with 7,8-BF plus DES caused an enhancement of oxidative DES metabolism in vivo, leading mostly to highly polar, as yet unidentified products. From a consideration of various cytochrome P-450-associated enzyme activities, it is concluded that the observed effect on biliary DES metabolites is most likely to be due to an estrogen-induced intrahepatic cholestasis. Taken together, the data do not support a role for the metabolic activation of DES in this tumor model. Alternative mechanisms are proposed.

Animals↗
PubMed1988

Effect of pretreatment of male Syrian golden hamsters with 7,8-benzoflavone and with diethylstilbestrol on P-450 isoenzyme activities and on microsomal diethylstilbestrol metabolism.

Combined treatment of male Syrian golden hamsters with the synthetic estrogen diethylstilbestrol (DES) and 7,8-benzoflavone (7,8-BF) gives rise to a high incidence of hepatocellular carcinomas, whereas no such tumors are formed with DES alone nor with 7,8-BF alone. To determine whether alterations in DES metabolism may account for the observed hepatocarcinogenicity, we have studied the effect of pretreatment with 7,8-BF alone, DES alone and 7,8-BF plus DES on the levels of hepatic P-450 and cytochrome b5, on the activities of various P-450 isoenzymes and on microsomal DES metabolism. Hepatic P-450 content was significantly increased after pretreatment with 7,8-BF and decreased after DES, while combined pretreatment led to levels similar to those in untreated control animals. Hepatic cytochrome b5 was also elevated in 7,8-BF-treated hamsters; DES pretreatment had no effect, and combined pretreatment led to a slight increase. Four different substrates were used to probe P-450 isoenzyme activity. Aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin-O-deethylase (ECOD), 7-ethoxyresorufin-O-deethylase (EROD) and 7-pentoxyresorufin-O-dealkylase (PROD) were all elevated after 7,8-BF-pretreatment, while DES led to a decrease in these activities with the exception of AHH, where a transient increase which was observed after 8 and 20 weeks of pretreatment was back to control levels after 32 weeks. Combined pretreatment with 7,8-BF and DES led to an intermediate response (slight increase) with AHH, EROD and PROD, but not with ECOD, where a full induction comparable with that observed after 7,8-BF alone was elicited. In spite of the modulation of enzyme levels and activities observed after the various pretreatments, the metabolism of DES in microsomes from pretreated animals was virtually identical with that from controls. Therefore it is concluded that modulation of hepatic DES metabolism is not the reason for the observed hepatotumorigenicity; instead, it is speculated that 7,8-BF is the carcinogenic agent in this tumor model, and DES may act as a promotor.

Animals↗
PubMed1985

Differential effects of 7,8-benzoflavone on polycyclic aromatic hydrocarbon dependent mutagenesis and cytotoxicity in a keratinocyte cell-mediated mutation assay.

A murine keratinocyte cell-mediated mutagenesis assay was used to examine the effects of 7,8-benzoflavone (7,8-BF) on the metabolic activation of 7,12-dimethylbenz[a]anthracene (DMBA) and benzo[a]pyrene (BP) to mutagenic and cytotoxic metabolites. DMBA-dependent mutagenesis and cytotoxicity were strongly and coordinately inhibited by 7,8-BF in a concentration-dependent manner. BP-dependent mutagenesis was also strongly inhibited by 7,8-BF in a concentration-dependent manner; whereas BP-dependent cytotoxicity was relatively unaffected by 7,8-BF. Maximum inhibition of DMBA- and BP-dependent mutagenesis occurred when the cultured keratinocytes were treated with 7,8-BF immediately prior to the addition of BP or DMBA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

In vivo effect of 7,8-benzoflavone on aryl hydrocarbon hydroxylase activity of mouse liver microsomes.

In vivo administration of 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produced much higher hepatic microsomal aryl hydrocarbon hydroxylase (AHH) induction than 7,8-benzoflavone (7,8-BF) in both aromatic hydrocarbon (Ah)-responsive and nonresponsive strains of mice. Simultaneous treatment or pre-treatment with 7,8-BF produced an inhibitory effect on AHH induction by MC or TCDD (i.e., the degrees of the inhibition, with TCDD, were 28% in the Ah-responsive strain C57BL/6N (C57) mice and 45% in the nonresponsive strain DDD;Qdj (DDD) mice). However, posttreatment with 7,8-BF was inclined to promote the induction of AHH by MC or TCDD (i.e., the degrees of the enhancement, with MC, were 15% in C57 mice and 45% in DDD mice). These results may suggest that the inhibitory effect of 7,8-BF in vivo is limited not to the combination of AHH inducer (MC or TCDD) but to its application of timing or Ah responsiveness.

Animals↗
PubMed2002

Prevention of chronic alcohol and nicotine-induced azospermia, sterility and decreased libido, by a novel tri-substituted benzoflavone moiety from Passiflora incarnata Linneaus in healthy male rats.

Excessive long term consumption of alcohol and nicotine have serious detrimental effects upon the libido, fertility, and sperm count in male species. The present work describes the beneficial effects of a novel tri-substituted benzoflavone moiety (BZF) isolated from Passiflora incarnata Linneaus, the phyto-chemical isolation, spectroscopic elucidation, and multifarious biological activities of which have recently been reported by the authors. The BZF moiety has been reported to increase libido, sperm count, and sexual fertility in 2 years old male rats at 10 mg/kg, po dose, in the one of our previous studies. Presently, the BZF moiety has been evaluated against chronic ethanol- and nicotine-induced decrease in libido, sexual fertility and mating efficiency in healthy male rats. The male rats were given ethanol (3 g/kg, po) A, nicotine (2 mg/kg, sc) N, alcohol-nicotine combinations (AN) alone, and also with 10 mg/kg po dose of BZF (concurrent administrations). These treatments were given for 30 days. At the end of treatments, it was observed that rat groups A, N, and AN had no libido (evaluated by mounting behaviour), declined sperm count, and consequently no mating efficiency or fertility (upon pairing with pro-estrus female rats). However, the rats which were given 10 mg/kg BZF along-with nicotine (NP group), alcohol (AP group), and alcohol-nicotine combination (ANP) exhibited significant libido-oriented mounting behaviour, increased sperm count (significantly comparable to the control group), and increased fertilization potential. The rats having decreased sperm count, libido and fertilization potential due to chronic administration of alcohol, nicotine and alcohol-nicotine combinations, i.e., rats of A, N, and AN groups were again subdivided and were given 10 mg/kg BZF for 7 days. This treatment confirmed that BZF speeds up the restoration of sexuality in rats upon cessation of the administration of substances like alcohol, nicotine and alcohol-nicotine combinations, which have severe detrimental effects upon male sexuality, fertility and vigour. BZF, the strongest inhibitor of aromatase enzyme, when administered concurrently with substances like alcohol and nicotine restores sexual virility, libido and vigour in male rats by maintaining the blood-testosterone levels to be high.

Alcoholism↗
PubMed2003

Restoration of chronic-Delta 9-THC-induced decline in sexuality in male rats by a novel benzoflavone moiety from Passiflora incarnata Linn.

1 The present study comprised treatment of healthy male rats with Delta(9)-tetrahydrocannabinol (THC, 10 mg kg(-1), p.o.), and combinations of THC with benzoflavone moiety (BZF, 10 and 20 mg kg(-1), p.o.) isolated from Passiflora incarnata Linneaus, over a period of 30 days. 2 Upon 30-days chronic administrations, the THC-treated male rats had a significant loss of libido (mounting behaviour with non-oestrous female rats), decrease in sperm count, and number of impregnated pro-estrous female rats. 3 Co-administration of BZF (10 and 20 mg kg(-1) p.o.) afforded significant protection against the chronic-THC-induced decrease in libido, mating performance and fertility during 30-day experimental regimen. The 20 mg kg(-1) dose of BZF exhibited better results. 4 Upon discontinuation of THC, treatment with BZF (10 and 20 mg kg(-1) p.o.) also facilitated the early restoration chronic-THC-induced decline in libido, sperm count and sexual fertility within 7 days.

Animals↗
PubMed2002

Nicotine reversal effects of the benzoflavone moiety from Passiflora incarnata Linneaus in mice.

A benzoflavone moiety (BZF) has recently been reported to be liable for many of the biological effects of the plant Passiflora incarnata Linneaus. In light of various reports mentioning the usefulness of P. incarnata in tobacco addiction, studies have been performed using four doses (1, 5, 10 and 20 mg/kg) of the bioactive BZF moiety isolated from the aerial parts of P. incarnata. In a 7-day experimental regimen, mice (n = 5) were given nicotine hydrogen tartrate (2 mg/kg), and combinations of nicotine with four doses of BZF (NnP-1, NnP-5, NnP-10 and NnP-20) q.i.d. by the s.c. route. At the end of the 7 days of treatment, naloxone was given to the mice from all groups to induce a nicotine withdrawal syndrome. The mice that had been treated with 10 and 20 mg/kg dose of BZF concurrently with nicotine showed a significantly fewer number of withdrawal jumps relative to the group treated with nicotine alone (Nn group). Separately, in a 14-day treatment regimen, mice (n = 10; for the N group, n = 12) were administered nicotine (2 mg/kg) and combinations of nicotine with four doses of BZF (NP-1, NP-5, NP-10, NP-20 groups) q.i.d. by the s.c. route. Spontaneous physical and behavioural signs of nicotine dependence were observed 3 hours after cessation of treatments on the 14th day. Mice administered with combinations of nicotine and 5, 10 and 20 mg/kg doses of BZF (i.e. NP-5, NP10 and NP-20 groups), exhibited less intensity and severity of withdrawal effects compared to the mice treated with nicotine alone. Those mice treated with the two highest doses of BZF,in combination with nicotine (NP-10 and NP-20), showed significantly fewer nicotine-abstinence withdrawal jumps and normal ambulatory behaviour. BZF treatment prevented weight loss and resulted in normal performance in the swimming endurance test, which may be a measure of stress and/or depression. Similarly, acute administration of a single 20 mg/kg dose of BZF prevented some of the nicotine-withdrawal effects; lower doses were almost inert. These studies, although preliminary, suggest that the BZF may have value in treating nicotine addiction.

Animals↗
PubMed2002

Beneficial effects of chrysin and benzoflavone on virility in 2-year-old male rats.

This work describes the potential usefulness of bioflavonoids for countering the deleterious effects of aging on male sexuality in 2-year-old rats. A flavone chrysin from Passiflora caerulea Linn. and a benzoflavone moiety (BZF) recently isolated from Passiflora incarnata Linn. were administered to 2-year-old male rats for a period of 30 days. After cessation of these treatments, there was a significant improvement in overall sexual functions in the rats given bioflavonoids, compared with control rats. The rats receiving chrysin (1 mg/kg) and BZF (10 mg/kg) exhibited increased libido when they were allowed to interact with nonestrous female rats. Additionally, both treated groups had increased sperm count, greater fertilization potential, and greater litter size when they were allowed to interact with proven proestrous female rats of a similar strain. BZF was more potent than chrysin as an antiaromatase agent and exhibited better effects on the sexual system of the 2-year-old male rats. Plant flavonoids have great potential for clinical and therapeutic applications against the physiological and biochemical effects of aging.

Aging↗
PubMed1990

Modification of 7,8-benzoflavone metabolism in hamster liver and kidney microsomes by hepatic tumor inducing treatments.

The effect of pre-treatment of male Syrian golden hamsters with 7,8-benzoflavone (BF), with diethylstilbestrol (DES) and with BF plus DES on the metabolism of [14C]BF in hepatic and renal microsomes has been studied in vitro. Whereas hepatic microsomes from DES-treated animals produced the same pattern of BF metabolites as control microsomes, a marked quantitative and qualitative alteration of BF metabolism was observed with liver microsomes from animals pre-treated with BF and with BF plus DES: the metabolic rate was increased and three new metabolites were formed which were not observed with control hepatic microsomes. These metabolites, which were tentatively identified as BF-5,6-dihydrodiol and two isomeric dihydroxy-BFs, were not detected in incubations with renal microsomes under any pre-treatment regimen. Non-extractable binding of radioactivity to hepatic and renal microsomal protein was observed in all incubations but did not exhibit as pronounced a dependence on pre-treatment as did the pattern of BF metabolites. Based on the metabolic data it is concluded that BF induces its own oxidative metabolism. Among the metabolites are reactive intermediates that bind to cellular macromolecules and may play an important role in tumor formation in the male Syrian hamster liver following prolonged treatment with BF plus DES.

Animals↗
PubMed1990

Induction of cytochrome P450IA1 in rat colon and liver by indole-3-carbinol and 5,6-benzoflavone.

It is known that consumption of cruciferous vegetables protects against the chemical induction of cancer in many organs. It has been suggested that this protection is mediated through an effect on the cytochrome P450 monooxygenase system. This system is responsible for the activation of a number of chemical carcinogens to their ultimate forms. In the present study, the effect of indole-3-carbinol (I3C) and 5,6-benzoflavone (5,6BF) on the expression of cytochrome P450IA1 in rat colon and liver has been investigated. Cytochrome P450IA1 mRNA was induced in colon following a single oral administration of I3C or 5,6BF. A biphasic induction profile was obtained with maxima at 4 and 16 h post-administration. Both inducers caused an approximately 2-fold increase in P450IA1 mRNA at 4 h and a 10-fold increase at 16 h. In contrast, both cytochrome P450IA1 and IA2 mRNAs was increased over the control between 4 and 24 h. The total amount of P450IA mRNAs in liver at 4 and 16 h was increased about 2- and 4-fold respectively by I3C; 5,6BF induced the P450IA mRNAs 4- and 5-fold respectively. The expression of cytochrome P450IA1 and IA2 is induced by I3C and several flavones present in cruciferous vegetables. This suggests that one of the protective effects of cruciferous vegetables in the reduction of chemically induced cancer may be regulation of cytochrome P450s involved in the metabolism of the chemical carcinogens.

Animals↗