Laser photodynamic therapy for papilloma viral lesions.

Photodynamic therapy was tested for its therapeutic efficacy in eradicating rabbit papilloma warts. The wild-type viral warts suspension was used to induce treatable papilloma warts in the cutaneous tissue of Dutch Belted rabbits. The photosensitizing agents used intravenously were Photofrin II at 10 mg/kg of body weight and Chlorin e6 monoethylene diamine monohydrochloric acid (Chlorin e6 med HCl) at 1 mg/kg of body weight. The lasers used were an argon-dye laser at 628 and 655 nm and a gold vapor laser at 628 nm. The irradiances of 25 to 180 mW/cm2 were applied topically with an end-on lens optical fiber with total radiant doses of 7.5 to 54 J/cm2. Photofrin II and the argon-dye laser at the highest light dosage (54 J/cm2) and Chlorin e6 monoethylene diamine monohydrochloride administered 2 hours before argon-dye laser irradiation at 655 nm at the highest light dosage (54 J/cm2) produced wart regression. Total wart regression without recurrence was achieved with Photofrin II and the gold vapor laser at all light dosages. The difference observed between the argon-dye laser and the gold vapor laser might be explained by the pulsed nature of the gold vapor laser, with its high-peak powers, some 5000 x the average measured light dose. In this model, the smaller, less cornified lesions were more effectively treated with photodynamic therapy.

Induction of nuclear aberrations by smokeless tobacco in epithelial cells of human oral mucosa.

Cytologic and cytogenetic studies were performed to assess the prevalence of somatic cell genetic damage in 48 young adults equally divided to represent users and nonusers of smokeless tobacco. Exposure was ascertained by measuring saliva cotinine using capillary gas chromatography. Squamous epithelial cells sampled from the oral mucosa demonstrated significant cytologic alterations associated with tobacco exposure. The frequency of micronucleated cells was significantly (P less than .01) higher in the labial mucosa of exposed (2.22%) compared to unexposed (0.27%) individuals. The frequency of micronuclei varied widely between exposed subjects but was higher in heavily (2.48%) compared to lightly (1.29%) exposed individuals as measured by saliva cotinine levels. Morphologic classification of epithelial cell nuclei showed that the frequency of cells with normal nuclear structure was significantly (P less than .01) reduce in exposed individuals. Analysis of oral epithelial cells of five additional nonusers of smokeless tobacco but wearers of orthodontic appliances to stimulate abrasion demonstrated no difference from the nonexposed control group. Unlike the case with cigarette smokers, peripheral lymphocyte sister-chromatid exchange frequency was not affected by exposure to smokeless tobacco. The oral cytology data, however, support an interpretation of exposure-dependent nuclear alterations, including micronuclei, in the oral epithelium associated with the use of smokeless tobacco. Altogether, results suggest that use of smokeless tobacco may cause genetic damage to cells in the oral epithelium.

Induction of sister-chromatid exchanges in vivo in mice by the mycotoxins sterigmatocystin and griseofulvin.

Two naturally occurring fungal mycotoxins, sterigmatocystin and griseofulvin, were tested for induction of sister-chromatid exchanges (SCEs) in bone marrow cells of female Swiss albino mice. Sterigmatocystin gave elevated SCE frequencies at all doses tested (0.06-6.0 mg/kg). In contrast, griseofulvin, tested from 0.4 to 200 mg/kg, elevated the SCE frequency only in those mice which received doses of 100 or 200 mg/kg body weight. These results indicate that both fungal mycotoxins induce SCE in vivo and are potentially mutagenic.