The ultra violet co mpon ent of sunli ght is the major ca use of skin cancer and is res ponsible for accelerating the aging of human sk in. It is th erefore important to determine the mechanisms by which ultraviolet li g ht alters normal cellular fun ctions. The potenti al importance of ultraviolet lig ht-indu ced dama ge to non-DNA targets has received little attention. Since the cy toskeleton is ;;. n im portant particip ant in the control of normal cell g row th, the Hlicro-E pide miologic

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... d ex perim ental evidence has esta blished solar ultravio let (UV) li g ht as the major ca use of skin ca nce r [1 ,2]. C hron ic ex posure to sunlig ht also damages derma l co nn ective ti ss ue and contributes to the agin g of hum an skin [3, 4] . A g rea t deal of effort has therefore been expend ed tr ying to elu cidate th e m echanism s by which UV li ght alters no rmal cellul ar fun cti o ns. The majority of past inves ti gation s ha ve exa min ed DNA da m age resulting from exposure to short waveleng th UV li g ht . This has left man y investigators with th e impression th at pyrimidine dim ers are the sole lesion res ponsible for solar ca rcinogenes is. Hum ans are not exposed to such short wavelength UV li g ht, however, sin ce vvavelen g ths below 290 nm do no t penetrate the atmosp heric ozone laye r. Furtherm o re, th e transformation of norm al cells to a cancerOus pheno ty pe appea rs to be a co mplex multistep process, ITlost o ften described as in volving stages of initiati o n and pro-ITlotion [5,6]. C urrent experim ental evid ence suggests that initia tion is ca used by geneti c dam age, and that promotion res ults fro m epigene ti c events. Since ex posure to promoters is not required for tumor induction by "compl ete" carcinogens, most in ves ti ga ti o ns into the ca rcinogeni c properties o f UV li ght continu e to emphas ize its genoto xic ca pability. [s it likely th at UVB-(290-320 n111) o r UV A-(320-400 nm) indu ced alte rations of non-DNA targets ma y contribute to the d evelo pm ent of cellular d ysfun cti o ns? It has bee n known for m an y yea rs tha t environmental waveleng ths of UV li g ht induce bi ologicall y important lesions at no n-DN A sites in bacterial cells [7] . M anu script Abbreviations: HBSS: Hanks' balanced salt solution PB S: phosphate-buffered saline UV : ultra viole t UVA: 320-400 11m UV light UVB : 290-320 11m UV li ght UV C: 200-290 nm UV li ght fil am ents and micro tubules of UV irradiated human skin fibrobla sts have been studi ed usin g fluorescence microsco py. Polychromatic ultraviolet li g ht, co mposed of environm entall y relevant wavelengths, was found to disrupt th e cytoplas mi c mi cro tubul e complex in a dose dependent m ann er. The indu ction of mi cro tubul e disasse mbl y did not co rrelate with the cyto toxi city of ultraviol et li g ht of varying compositi on. J Ill ves t Deml(l/o/ 89:603-606, 1987 Evidence has begun to acc umul ate in m ammalian cell studies that les ions other th an pyrimidin e dimers m ay be in volved in the carcinogeni c, mutageni c, and leth al effects of solar UV li g ht [S-15]. Alth o ug h in ves ti gato rs continue to seek additio nal DNA lesions to explain thesc findings, the importa nce of damage to other cellular co mpon ents must also be considered. The cyto plasm of eukaryo ti c cell s contain s an intricate network of fi lamentous stru ctures th at arc co llectively refe rred to as the cytoskeleton. The three m ajo r components of the cytoskeleton arc mi crotubules, mi cro fil am ents and interm edi ate fil ame nts /1 6). Since the cytos keleton is an important participant in the contro l o f no rmal cell g rowth , we have begun to explo re the possibility that UV li ght m ay indu ce cy toskeletal ch anges. We have been particularly interested in cytoskele tal alteratio ns indu ced by po lychro m atic UVB and UV A li g ht sources, sin ce they m o re closely simulate the UV li g ht to w hi ch we are ro utinel y ex posed. Co mpari sons have also been m ade w ith the m o re co mm o nl y investigated, 254 nm UV li g ht. MATER IALS AND METHODS Cells AG1522, o bta ined from the In stitute for M ed ica l Resea rch (Ca mden, N ew J ersey), is a no rm al, dip loid hum an sk in fibrob las t cell strain . Cells we re g rown in Eagle's minim al essential m edi um (G ibco, Grand Island , N ew Yo rk) supplemented w ith 10% fetal calf se rum , 0.9 gi l D-g lucose, 0.66 m g/l sodium py ru vate, 11 0 U / ml penicillin and 110 ug / ml strepto m yc in s ul fa te. C ultures we re in cubated at 37°C in :1n at m osphe re of 95% air: 5% CO 2 , UV Light General E lectric GST5 germicidal lam ps, Westingho use FS40 lamps, and Sylvania FR40T12 lamps were our sources of UV C, sun lamp, and UV A li g ht, respectively. T he UVC lamps emit grea ter th an 95 % of their energy at 254 nm. The spectra of li g ht transmitted by the Westinghouse FS 40 and Sy lva nia FR40T12 lamps thro ug h po lysty rene culture dish covers have been published [1 7]. BrieRy , the sun la mps transmit approx im ately equa l am o unts of li g ht in the UVB and UVA wavebands , with a peak emissio n in the UVB reg io n betwee n 3 10 and 315 nm . More th an 9S% of th e li g ht fro m the UVA la mps, w hi ch e mit nu xim all y at 350-355 nm, is in the UV A wave band . UVC dose rates we re determin ed w ith an Inte rnatio nal Li g ht (N ew burypo rt, M assachusetts) IL 254 germi cidal photometer. Su n lamp and UV A dose rates we re determined w ith an lnter-0022-202X / 87/ S03.50 Copyri ght