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Biomedical subjects

F J Akin

Publications and source records attributed to F J Akin.

At least 19 recordsLinked to original sources
PubMed1985

The contributions of UVA and UVB to connective tissue damage in hairless mice.

UVA, in high-dose single exposures, can, like UVB, be deleterious to skin. Dermal damage resulting from chronic exposure to UVA has not been studied. To investigate the long-term effects, we irradiated albino hairless mice for 30-34 weeks with UVA radiation, alone, from two sources with differing spectral qualities, and in combination with UVB as solar-simulating radiation. The results were compared to UVB alone. Like UVB, the UVA waveband, especially that with a spectral distribution similar to solar UVA, caused elastic fiber damage, increased glycosaminoglycan levels, and produced hypertrophy of deep dermal tissues. There were, however, striking differences between UVB- and UVA-irradiated skin. A combination of UVA and UVB summated the effects of both wavebands. Substantial protection against these effects was afforded by a broad-spectrum sunscreen.

Animals↗
PubMed1983

Sunscreens promote repair of ultraviolet radiation-induced dermal damage.

Chronic UV irradiation profoundly damages the dermis of human and animal skin. These alterations were thought to be irreversible. Recently, we showed that substantial repair occurred in hairless mice after stopping UV exposure. A band of new connective tissue was laid down subepidermally. The present study focussed on whether repair would occur if animals were protected by sunscreens after dermal damage was induced and irradiation was continued. Albino hairless mice were exposed to Westinghouse FS20 sunlamps thrice weekly for 30 weeks. The daily dose of UV (UVB + UVA) was 0.17 J/cm2. Sunscreens of sun protection factors (SPF) 6 and 15 were applied after 10 and 20 weeks of irradiation. Biopsies were taken at 10, 20, 30, and 45 weeks of the experiment. With both sunscreens, especially SPF-15, previously damaged dermis was repaired during continued irradiation. Repair occurred in situ and, in severely damaged skin, in the novel form of subepidermal reconstruction zones of new connective tissue with parallel collagen bundles and a network of fine elastic fibers.

Animals↗
PubMed1982

Prevention of ultraviolet damage to the dermis of hairless mice by sunscreens.

To assess the ability of sunscreens to protect connective tissue from actinic damage, hairless mice were irradiated with Westinghouse FS20 sunlamps thrice weekly for 30 weeks. Each exposure, consisting mainly of UV-B and the less energetic UV-A, was approximately 6 human minimal erythema doses under these lights. One group of animals received irradiation only. The other 2 groups were treated, prior to irradiation, with sunscreens of either low or high sun protection factors (SPF 2 and SPF 15, respectively). Skin biopsies were taken at 10-week intervals and were stained with various histochemical stains to reveal changes in the dermis. The unprotected, irradiated animals showed a great increase in the following: reticulin fibers, elastic fibers to the extent of elastosis, neutral and acid mucopolysaccharides and melanin production. The SPF 15 sunscreen completely prevented these changes. The SPF 2 sunscreen was less effective. These effects were substantiated by ultrastructural examination of the tissues by electron microscopy. A surprising histologic finding was the repair capability of the dermis in the post-irradiation period.

Animals↗
PubMed1981

Changes in epidermal forward scattering absorption after UVA or UVA-UVB irradiation.

Groups of skh-1 (albino) and Skh-2 (pigmented) hairless mice were irradiated for 125 hr using a modified GE F8T5-BL black light with and without a 3-mm plate glass filter to remove light below 320 nm. The epidermis was examined by forward scattering and by histological section postirradiation at 48 hr, 96 hr, 9 days, and 23 days. Changes in the epidermis of all animals were compared to control groups. Although no differences were seen between Skh-1 and Skh-2 mice, both the magnitude and shape of the forward scattering absorption curves were changed by the irradiation used. In both strains, differences which were detected at 48 hr postirradiation had returned to normal visually by 23 days, with no augmented pigmentation occurring in Skh-2 animals. At 23 days postirradiation, however, residual optical alterations were observed. This phenomenon, detected optically, may be skin acclimatization.

Absorption↗
PubMed1980

Sunscreens prevent ultraviolet photocarcinogenesis.

Sunscreens of low or high sun protection factors (SPF*) were tested for their ability to inhibit ultraviolet (UV) carcinogenesis in two varieties of hairless mice. Low protection (SPF = 2) reduced by 50% the number of albino animals developing tumors. High protection (SPF =15) prevented tumor formation. Tumorigenesis was totally prevented in the lightly pigmented variety with either sunscreen, demonstrating the added protection of melanin. In mice and man, UV-induced cancer is a cumulative process. Reducing the amount of UV light reaching the basal layer will retard that process.

4-Aminobenzoic Acid↗
PubMed1976

Identification of polynuclear aromatic hydrocarbons in cigarette smoke and their importance as tumorigens.

Fraction F20, which in other studies was the most tumorigenic neutral fraction of cigarette smoke condensate (CSC), was separated by gel filtration chromatography into refined subfractions for identification of the polynuclear aromatic hydrocarbons (PAH) and for bioassay on mouse skin. Several hundred PAH were positively identified. Subfraction F55. containing most of the carcinogenic PAH as well as numerous unidentified components, was almost as tumorigenic to 7,12-dimethylbenze[a]anthracene (DMBA)-pretreated female outbred CD-1 mice as was F20. When F55 was separated into two parts, the first containing unidentified material (F55A) and the second containing the PAH (F55B), neither was significantly tumorigenic. F55B, combined with two other active fractions from the neutral and the acidic portions of CSC, exhibited a synergistic tumorigenic effect on DMBA-pretreated mice. The results supported the concept that the PAH in cigarette smoke must interact with other components in order to exert a tumorigenic effect.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Factors affecting measurement of aryl hydrocarbon hydroxylase activity in mouse skin.

Mouse skin exhibits relatively high aryl hydrocarbon hydroxylase (AHH) activity when measured under optimal conditions. The enzyme is unequally distributed in the cutaneous layers with the highest concentration in the epidermis. Subcellularly, it is localized in the microsomal fraction. As much as two-thirds of the enzymatic activity was destroyed when harsh homogenization techniques were used during tissue preparation. Incorporation of the reduced pyridine nucleotide NADH into an incubation mixture containing NADPH increased epidermal AHH activity by one-third. When methods that maximize activity were employed, the AHH activities of skin of C57BL/6 inbred mice and of ICR Swiss random-bred mice were 5 to 10 times as active as lung tissue and about one-tenth as active as liver.

Animals↗
PubMed1975

Mouse skin tumorigenesis and induction of aryl hydrocarbon hydroxylase by tobacco smoke fractions.

Ten fractions separated from the neutral portion of cigarette smoke condensate (CSC) were tested on mouse skin for tumor-initiating activity and for their capacity to induce the enzyme aryl hydrocarbon hydroxylase (AHH). Tumor-initiating activity was confined primarily to the fraction containing more than 90% of the polynuclear aromatic hydrocarbons (PAH) in CSC. One other PAH-containing fraction was active. The combined initiating effect of these fractions was comparable to that of a 40-ppm solution of benzo[a]pyrene (BP), which is about 40 times the BP content of CSC. Some of the neutral fractions that have been demonstrated to cause tumor promotion in mice pretreated with 7,12-dimethylbenz-[aA1ANTHRACENE sere inactive as tumor initiators. The fractions that contained aromatic hydrocarbons induced mouse skin AHH levels twofold to sixfold after a single topical application. AHH-inducing activity was not, however, a reliable indicator of the carcinogenic potential of a fraction.

Animals↗