Inhibitory activity of tannic acid and flavonols on the infectivity of Herpesvirus hominis and Herpesvirus suis.
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Antiviral Agents↗
Biomedical subjects
R Pusztai
Publications and source records attributed to R Pusztai.
Antitumor activity of benzo[a]phenothiazines.
We have previously reported on the diverse biological activities of benzo[a]phenothiazines, such as the induction of antitumor and antimutagenic activity in vivo, and differentiation and apoptosis in vitro. The relationship of radical generation and pi-spin density or dipole moment was investigated, using quantum-chemical calculation with UHF/PM3. These data suggest that the origin of radical generation by active benzo[a]phenothiazines, which affect such biological activities might be N-atom at position 12.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Membrane associated antitumor effects of crocine-, ginsenoside- and cannabinoid derivates.
In the present work a systematic study was initiated with crocine, ginsenoside and cannabinoid derivatives on multidrug resistant mouse lymphoma cells, viral tumor antigen expression and some human leukocyte functions. Among saffron derivatives, crocin and picrocrocin, triglucosyl and diglucosyl crocetin were ineffective on the reversal of multidrug resistance of lymphoma cells. Ginsenoside increased drug accumulation and tumor antigen expression at 2.0-20.0 micrograms/mL. Some cannabinoid derivatives such as cannabinol, cannabispirol and cannabidiol increased drug accumulation, while cannabidiolic acid, delta-9-THC and tetrahydro-cannabidiolic acid reduced drug accumulation of the human mdr1-gene transfected mouse lymphoma cells. The reversal of multidrug resistance is the result of the inhibition of the efflux pump function in the tumor cells. Crocetin esters were less potent than crocin itself in the inhibition of EBV early antigen expression. However crocin and diglucosylcrocetin inhibited early tumor antigen expression of adenovirus infected cells, but triglucosylcrocetin was less effective at 0.01-1.0 microgram/mL. The crocin had no antiviral effect [on HSV-2 infected vero cells] up to 25 micrograms/mL concentration. Ginsenosides had a moderate inhibitory effect except ginsenoside Rb1 (was the less effective) on the drug efflux pump. Among the cannabinoid derivatives the cannabinol and cannabispirol increased drug accumulation, while cannabidiolic acid and delta-8-THC, delta-9-THC and tetrahydro-cannabinol reduced drug accumulation in multidrug resistant mouse lymphoma cells. It is interesting that ginsenosides had a chemical structure-dependent immunomodulating effect by enhancing the activity of NK-cells and ADCC activities.
Animals↗
Effect of tannic acid on different viruses.
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Adenoviridae↗
[Molecular aspects of interferon induction by adenoviruses].
The capacity of adenovirus to induce interferon in the infected cells was studied. The examined adenovirus strains of early types were grouped in 2 groups according to their capacity to induce interferon and to the sensitivity of the infecting and interferon-inducing activity to UV-irradiation. A common property of adenoviruses, potent interferon inducers, is their high sensitivity to UV-irradiation.
Adenoviruses, Human↗
Effects of two benzo[a]phenothiazines on multi-drug resistance (mdr) and tumor antigen expression.
Two benzo[a]phenothiazines 5H-benzo[a]phenothiazin-5-one (1), and its derivative 6-methyl-5H-benzo[a]phenothiazin-5-one (2) inhibited the proliferation of human and mouse tumor cell lines. The multi-drug resistant (mdr) subline was more sensitive than its parent cell line to 5H-benzo[a]phenothiazin-5-one (1), 6-methyl-5H-benzo[a]phenothiazin-5-one (2) was equally antiproliferative against the three cell lines tested. Rhodamine 123 efflux of mdr cells was more efficiently inhibited by 5H-benzo[a]phenothiazin-5-one (1) than by 6-methyl-5H-benzo[a]phenothiazin-5-one (2). The exposure of adenovirus infected cells to 5H-benzo[a]phenothiazin-5-one (1) resulted in a reduction of tumor-antigen expression, whereas 6-methyl-5H-benzo[a]phenothiazin-5-one (2) enhanced the T-antigen expression.
Animals↗
Relationship between tumor (T) antigen expression and substituent effects on benzo [a] phenothiazines.
Human adenovirus, oncogene-type 12 infected HEp-2 cells were exposed to six benzo[a]phenothiazines. 5-Oxo-5H-benzo[a]phenothiazine (4) and 6-hydroxy-5-oxo-5H-benzo[a]phenothiazine (5) were moderately toxic. 9-Methyl-12H-benzo[a]phenothiazine (2), 10-methyl-12H-benzo[a]phenothiazine (3), 6-methyl-5-oxo-5H-benzo[a]phenothiazine (6), and 12H-benzo[a]phenothiazine (1) were not toxic in the system tested. 6-Methyl-5-oxo-5H-benzo[a]phenothiazine (6) enhanced the expression of viral oncogene product (tumor antigen) in the adenovirus infected cells. 5-Oxo-5H-benzo[a]phenothiazine (4) and 6-hydroxy-5-oxo-5H-benzo[a]phenothiazine (5) reduced this effect. 6-Methyl-5-oxo-5H-benzo[a]phenothiazine (6), with hyperconjugation due to the methyl group, increased the T antigen activity at higher dose concentrations, whereas 6-hydroxy-5-oxo-5H-benzo[a]phenothiazine (5) with a hydroxy substituent had the opposite effect on T antigen expression. The methyl substitution at positions C9 or C10 increased the T antigen expression of adenovirus infected cells.
Antigens, Neoplasm↗