Means ± standard deviation (SD) of histidine revertant colonies, mutagenic index (MI), and inhibition percentage (IP) of mutagenicity for two tester strains of <i>Salmonella typhimurium</i>, TA98 and TA100, after treatment with different doses of sulfonamide chalcone N-{4-[3-(4-nitrophenyl)prop-2-enoyl]phenyl}-benzenesulfonamide (CPN).

<p>¹ Negative control: 20 μL dimethylsulfoxide (DMSO).</p><p>² Positive control: 0.5 μg 4-nitroquinoline 1-oxide (4-NQO)/plate for TA98 and 1.5 μg sodium azide/plate for TA100.</p><p>All values are means ± SD of three independent experiments.</p><p>³ Statistical analysis: one-way ANOVA and the Tukey’s test.</p><p>^{a, b, c, d} Letter in common in the same column do not present significant difference (<i>p</i> > 0.05). Different letters in the same column present significant difference (<i>p</i> < 0.05).</p><p>Means ± standard deviation (SD) of histidine revertant colonies, mutagenic index (MI), and inhibition percentage (IP) of mutagenicity for two tester strains of <i>Salmonella typhimurium</i>, TA98 and TA100, after treatment with different doses of sulfonamide chalcone N-{4-[3-(4-nitrophenyl)prop-2-enoyl]phenyl}-benzenesulfonamide (CPN).</p

Evaluation of cytotoxic and genotoxic activities in the bone marrow of mice treated with sulfonamide chalcone N-{4-[3-(4-nitrophenyl)prop-2-enoyl]phenyl}-benzenesulfonamide (CPN) based on MNPCE and PCE/NCE frequency.

<p>¹ Negative control: dimethylsulfoxide (DMSO) 0.1 mL/10 g body weight (b.w.).</p><p>² Positive control: mitomycin C (MMC) 4 mg/kg (80% LD₅₀).</p><p>All values are mean ± SD of five mice.</p><p>³ Statistical analysis: one-way ANOVA and the Tukey’s test.</p><p>⁴ Statistical analysis: chi-square (χ^<b>2</b>) test.</p><p>Mean values followed by the same letter in the column do not present significant difference at 5% probability.</p><p>^{a, b, c, d} Letter in common in the same column do not present significant difference (<i>p</i> > 0.05). Different letters in the same column present significant difference (<i>p</i> < 0.05).</p><p>Evaluation of cytotoxic and genotoxic activities in the bone marrow of mice treated with sulfonamide chalcone N-{4-[3-(4-nitrophenyl)prop-2-enoyl]phenyl}-benzenesulfonamide (CPN) based on MNPCE and PCE/NCE frequency.</p

Yield, physical state, melting point, purity, and spectroscopic data (GS-MS, IR, ¹H-NMR) of N-(4-acetylphenyl)benzenesulfonamide (1) and N-{4-[(<i>E</i>)-3-(4-nitrophenyl)prop-2-enoyl]phenyl}-benzenesulfonamide (2).

<p>¹ Retention time.</p><p>² Mobile phase used: CH₃CN:aqueous buffer containing chloroacetic acid 0.1% (55:45).</p><p>Yield, physical state, melting point, purity, and spectroscopic data (GS-MS, IR, ¹H-NMR) of N-(4-acetylphenyl)benzenesulfonamide (1) and N-{4-[(<i>E</i>)-3-(4-nitrophenyl)prop-2-enoyl]phenyl}-benzenesulfonamide (2).</p

Protective Effects of Silymarin and Silibinin against DNA Damage in Human Blood Cells

Silymarin (SM), a standardized extract derived from Silybum marianum (L.) Gaertn, is primarily composed of flavonolignans, with silibinin (SB) as its major active constituent. The present study aimed to evaluate the antigenotoxic activities of SM and SB using the alkaline comet assay in whole blood cells and to assess their effects on the expression of genes associated with carcinogenesis and chemopreventive processes. Different concentrations of SM or SB (1.0, 2.5, 5.0, and 7.5 mg/ml) were used in combination with the DNA damage-inducing agent methyl methanesulfonate (MMS, 800 μM) to evaluate their genoprotective potential. To investigate the role of SM and SB in modulating gene expression, we performed quantitative real-time PCR (qRT-PCR) analysis of five genes that are known to be involved in DNA damage, carcinogenesis, and/or chemopreventive mechanisms. Treatment with SM or SB was found to significantly reduce the genotoxicity of MMS, upregulate the expression of PTEN and BCL2, and downregulate the expression of BAX and ABL1. We observed no significant changes in ETV6 expression levels following treatment with SM or SB. In conclusion, both SM and SB exerted antigenotoxic activities and modulated the expression of genes related to cell protection against DNA damage

Characterisation of microbial attack on archaeological bone

As part of an EU funded project to investigate the factors influencing bone preservation in the archaeological record, more than 250 bones from 41 archaeological sites in five countries spanning four climatic regions were studied for diagenetic alteration. Sites were selected to cover a range of environmental conditions and archaeological contexts. Microscopic and physical (mercury intrusion porosimetry) analyses of these bones revealed that the majority (68%) had suffered microbial attack. Furthermore, significant differences were found between animal and human bone in both the state of preservation and the type of microbial attack present. These differences in preservation might result from differences in early taphonomy of the bones. © 2003 Elsevier Science Ltd. All rights reserved