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PubMedDate not supplied

Studies on the male antifertility agent--gossypol acetic acid. III. Effect of gossypol acetic acid on rat testis.

Gossypol acetic acid at the dose of 5 mg/rat/day for 2 and 4 weeks did not cause any significant effect on the body weight, testis, epididymis, seminal vesicle and prostate weight, nor gossypol treatment had any significant effect on the activities of acid phosphatase and succinic dehydrogenase in the testis. Changes in the testis ATPase activity were, however, significant after gossypol treatment. During the course of present investigations no effect of gossypol treatment on 3H thymidine incorporation into DNA of testicular cells was observed, nor there were any changes in the DNA and total protein content of the testis after gossypol treatment. Gossypol treatment did not cause any effect on the plasma Na+ level. However, transient decrease in the plasma K+ level was observed; decrease in K+ level two weeks after gossypol treatment was restored to normal after 4 weeks of gossypol treatment. No changes in the histology of the testis were observed 2 weeks after gossypol treatment but marked inhibition of spermatogenesis was observed 4 weeks after gossypol treatment. Motility of vas deferens spermatozoa was also markedly inhibited 4 weeks after gossypol treatment. In the light of the present observations and those of others, there is a clear demonstration that gossypol acts directly on the spermatozoa and on the testis; at both the sites the drug interferes in the ATPase activity.

Adenosine Triphosphatases↗
PubMed1992

Disappearance of acetic acid from the bovine reticulorumen at basal and elevated concentrations of acetic acid.

Disappearance of acetic acid was quantified to determine whether removal of this acid from the reticulorumen is altered when ruminal acetic acid concentrations are elevated. Ruminally fistulated beef steers (n = 3 per experiment; BW = 320 +/- 9 kg) were fed eight times daily a 46% corn-based concentrate:54% mixed hay diet to meet maintenance energy requirements (3.5 kg of DM/d). In situ production of acetic acid, determined by pulsed-continuous infusion of [1-14C]acetic acid, was 530 mmol/h (CV = 12%). Disappearance from the reticulorumen (i.e., presumed absorption) was 460 mmol/h (CV = 2%) or 87% (CV = 2%) of ruminal production. Variation is described within an operational steady state. Acetic acid concentrations were increased by continuous infusion of unlabeled acetic acid into the reticulorumen. Ruminal disappearance (mmol/h) increased when this simulated production was elevated up to and exceeding in situ rates reported previously (530 to 2,700 mmol/h). These data suggest that two-thirds to three-fourths of ruminal acetate production disappeared across the reticuloruminal wall when concentration was elevated; the complement exited from the rumen with the liquid phase. The reticulorumen has an additional capacity to remove acetic acid; however, it does so with an apparent reduced efficiency at higher production rates. Liquid out-flow may affect the efficiency of reticuloruminal disappearance. Sites distal to the rumen become quantitatively important when ruminal acetic acid concentrations are increased.

Absorption↗
PubMedDate not supplied

Studies on the male antifertility agent--gossypol acetic acid. V. Effect of gossypol acetic acid on the fertility of male rats.

Gossypol acetic acid was given to male rats at a dose of 7.5 mg/rat/day six days a week for ten weeks. After nine weeks of gossypol treatment no implantation sites were observed in the females mated with gossypol treated males. After ten weeks of gossypol treatment all the spermatozoa in the vas deferens were non-motile. Gossypol treatment did not affect the body weight and the weights of the accessory sex organs. Plasma LH and FSH levels, hCG binding in testis and succinic dehydrogenase (SDH) and adenosine triphosphatase (ATPase) activities in liver, kidney and testis were not affected by gossypol treatment. Histological observations of the testis revealed partial damage to the seminiferous tubules. Single high doses of gossypol did not induce significant changes in the body weight and weights of testis and accessory sex organs. ATPase activity in the testis was reduced significantly after gossypol treatment, the enzyme activity in liver and kidney, was however, affected at high doses only. Gossypol treatment had no effect on the histoarchitecture of the testis. Intratesticular administration of gossypol evoked localized damage in the testis. Gossypol treatment had no effect on I125 FSH binding to the rat testis homogenate in vitro.

Animals↗
PubMed1994

The morphological effects of the anti-tumor agents flavone acetic acid and 5,6-dimethyl xanthenone acetic acid on the colon 38 mouse tumor.

Flavone acetic acid and 5,6-dimethyl xanthenone acetic acid have a broad spectrum of anti-tumor activity in mice, and act by stimulating immune cells and inhibiting tumor blood flow, resulting in hemorrhagic necrosis within 24 hrs. To study the evolution of hemorrhagic necrosis, subcutaneous Colon 38 tumors were examined by light and electron microscopy from 30 min to 24 hrs after treatment with these agents, and measurements of tumor energy metabolites made. The results show that both agents cause apoptosis beginning at 30 min, and that by 4 hrs necrosis supervenes, accompanied by rupture of tumor blood vessels. The absence of early endothelial cell damage or thrombosis suggests that vessel rupture, and consequent loss of blood flow and energy metabolite depletion, is caused by loss of extravascular mechanical support by the tumor parenchyma.

Adenocarcinoma↗
PubMed1987

Factors involved in the anti-cancer activity of the investigational agents LM985 (flavone acetic acid ester) and LM975 (flavone acetic acid).

LM985 has been shown previously to hydrolyse to flavone acetic acid (LM975) in mouse plasma and to produce significant anti-tumour effects in transplantable mouse colon tumours (MAC). It has undergone Phase I clinical trials and dose limiting toxicity was acute reversible hypotension. Substantially higher doses of LM975 can be given clinically without dose limiting toxicity. We have investigated the activity of LM975 against a panel of MAC tumours and also the in vitro cytotoxicity of both LM985 and LM975 in two cell lines derived from MAC tumours. LM985 is considerably more cytotoxic than LM975 in vitro but increased length of exposure to LM975 results in improved activity. Single in vivo injection of LM975 showed no activity against the ascitic tumour MAC 15A, moderate activity against the s.c. poorly differentiated tumour MAC 13 and produced a significant growth delay in the well differentiated MAC 26. These latter responses were considerably enhanced by repeated injection 7 days later. Pharmacokinetic studies in mice following i.p. injection of LM985 demonstrated rapid degradation of LM985 to LM975 in the peritoneum. Length of exposure as well as drug concentration appear important factors in determining anti-tumour responses.

Adenocarcinoma↗
PubMedDate not supplied

Studies on the male antifertility agent gossypol acetic acid. VI. Effect of gossypol acetic acid on the fertility of bonnet monkey. Macaca radiata.

Gossypol acetic acid (4 mg/day/5 days a week) suspended in Tonoferon tonic was given to male bonnet monkeys, Macaca radiata, by oral route for 3 months. Marked reduction in the sperm count/ejaculate and sperm motility were observed after gossypol treatment; both motility and sperm count/ejaculate returned to the normal level 8-10 weeks after termination of gossypol treatment. The citric acid and fructose levels in the semen of gossypol treated monkeys were not different from those of the controls.

Animals↗
PubMed1979

Analysis of some older Scandinavian formulations of 2,4-dichlorophenoxy acetic acid and 2,4,5-trichlorophenoxy acetic acid for contents of chlorinated dibenzo-p-dioxins and dibenzofurans.

Ten samples of older formulations of 2,4,5-trichlorophenoxy acetic acid and 2,4-dichlorophenoxy acetic acid used in Sweden were analyzed for chlorinated dibenzo-p-dioxins and dibenzofurans. The analyses were performed with gas chromatography/mass spectrometry with a high resolution glass capillary column for maximum isomeric separation and sensitivity. The detection limit was 0.01-0.05 ppm. The amounts of contaminants were of the same order of magnitude as that found earlier in European samples with later production dates (late 1960s and 1970s).

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1977

Mechanisms of acylation of chymotrypsin by phenyl esters of benzoic acid and acetic acid.

The kinetics of the acylation of alpha-chymotrypsin by a series of substituted phenyl p-nitrobenzoates have been studied by stopped flow and conventional spectrophotometry. Electron withdrawal in the leaving group accelerates the rate of acylation, and the p value obtained for eight esters is +1.96. The pH- and pD-independent acylation rate constants are, respectively, 1.40 X 10(4) M-1S-1 and 1.23 X 10(4) M-1S-1 for p-nitrophenyl p-nitrobenzoate, and, respectively, 2.19 X 10(3) M-1S-1 and 1968 X 10(3) M-1S-1 for p-nitrophenyl benzoate at 25 degrees. An analysis of structure-reactivity results and kinetic solvent isotope effects indicates a mechanism for acylation by phenylbenzoates in which initial reaction is a nucleophilic attack by an imidazole of the enzyme (His 57). Subsequently, there is rapid transfer of the acylating group to the serine 195 from the acylimidazole species. The kinetic solvent isotope effects for acylation by p-nitrophenyl phenyl acetate and p-nitrophenyl phenyl acetate and p-nitrophenyl hydrocinnamate, in 5%, v/v, acetonitrile, are 1.3 and 2.0, respectively. The latter ester is inhibited more than is p-nitrophenyl benzoate when 5%, v/v, dioxane is substituted for 5%, v/v, acetonitrile as co-solvent. In the presence of 5%, v/v, dioxane a change in the kinetic solvent isotope effect to 1.7 is found for p-nitrophenyl benzoate and p-nitrophenyl phenylacetate while that for the analogous hysdrocinnamate ester is unaffected. The results for the latter substrate are in accord with a general base-catalysed mechanism. Electron-withdrawal groups in the phenyl ring of phenyl acetates accelerate the enzyme acylation yielding a leaving group p of 2.05. The kinetic solvent isotope effects for acylation by p-nitrophenyl thiolacetate and by p-nitrophenyl acetate are close to 2.0. The mechanism of acylation of chymotrypsin by phenyl acetates is not unambiguously defined using these data.

Acetates↗
PubMed1994

Induction of tumor necrosis factor-alpha messenger RNA in human and murine cells by the flavone acetic acid analogue 5,6-dimethylxanthenone-4-acetic acid (NSC 640488).

The investigational antitumor agent, 5,6-dimethylxanthenone-4-acetic acid (5,6-MeXAA; NSC 640488) induced greater expression of tumor necrosis factor-alpha (TNF-alpha) mRNA in murine spleen cells in vivo at its optimal dose of 27.5 mg/kg than flavone acetic acid (FAA; NSC 347512) at its optimal dose of 220 mg/kg. Up-regulation of TNF-alpha mRNA was obtained using 5,6-MeXAA in vitro in cultures of murine splenocytes, the murine J774 macrophage cell line, and the human HL-60 myelomonocytic leukemia cell line. Maximal induction occurred at a 5,6-MeXAA concentration of 200 micrograms/ml for both murine J774 and human HL-60 cells. A direct comparison of FAA and 5,6-MeXAA (100-600 micrograms/ml) to stimulate TNF-alpha mRNA in HL-60 cells showed activity by 5,6-MeXAA at all doses but minimal activity with FAA. The results demonstrate that 5,6-MeXAA is equally potent in up-regulating TNF-alpha mRNA in human and murine cells of the monocyte/macrophage lineage, whereas FAA has demonstrable activity in murine cells only. The results suggest that 5,6-MeXAA would be a more active clinical agent than FAA because TNF-alpha induction appears to be a critical factor in the antitumor effects of this class of compounds.

Animals↗
PubMed1993

Serotonin involvement in the antitumour and host effects of flavone-8-acetic acid and 5,6-dimethylxanthenone-4-acetic acid.

The relationship of serotonin (5-HT) receptors to the action of the experimental antitumour drugs flavone-8-acetic acid (FAA) and 5,6-dimethylxanthenone-4-acetic acid (5,6-MeXAA) was studied. Both FAA and 5,6-MeXAA are known to induce the synthesis of tumour necrosis factor-alpha (TNF) and to stimulate nitric oxide synthesis in vivo, as measured by elevation of plasma nitrate. Serotonin potentiated the effect of a subtherapeutic dose of 5,6-MeXAA (20 mg/kg) as measured both by plasma nitrate increase and by growth delay of s.c. implanted colon 38 tumours. On the other hand, administration of the serotonin 5-hydroxytryptamine-2 (5-HT2) antagonist cyproheptadine (20 mg/kg) inhibited both the plasma nitrate response and, to a lesser extent, the induction of tumour haemorrhagic necrosis by 5,6-MeXAA, FAA and TNF. Reduction of circulating plasma serotonin by pre-treatment with p-chlorophenylalanine and reserpine reduced the plasma nitrate response, but not the tumour necrosis response, to 5,6-MeXAA (30 mg/kg). It is suggested that serotonin is necessary for the induction of nitric oxide synthases and acts, either directly or indirectly, in concert with TNF. Serotonin agonists may have utility in increasing nitric oxide synthesis in response to TNF or to agents that induce TNF as part of their antitumour action.

Animals↗