CELL MEMBRANE COMPLEX 459 through beta-delta failure (32,33) and the resultant chipping of cuticle from the hair via abrasive actions. Cuticle loss in the wet state is primarily caused by the rupturing of cuticle cells internally and is greater in chemically damaged hair such as alkaline peroxide-treated or permanent-waved hair than in chemically untreated hair (84). Fatigue testing, a method developed at TRI-Princeton by Ruetsch, Kamath and, Weigmann (involving attaching a weight to a hair and dropping the weight multiple times to con- tinuously shock or jar the fi ber), shows that alkaline peroxide treatment of human hair fi bers when fatigued produces numerous scale-edge fractures with scale-edge chipping. Ruetsch (86) fatigue tested peroxide-treated hair, followed by extension, and found ex- tensive fracturing in the CMC between the scales due to a weakened cuticle–cuticle CMC. This effect is most likely due to peroxide attack on thioester linkages that disrupts the beta layers of the cuticle–cuticle CMC. Takahashi et al. (87) have provided evidence that wet cuticle wear in Asian hair is due more to CMC failure (possibly involving the central hydrophilic “contact zone” of the delta layer) rather than failure inside cuticle cells as in Caucasian hair (most likely endo- cuticular failure). Takahashi et al. (87) showed that wet cuticle wear on Asian hair occurs at a faster rate than on Caucasian hair because of differences in elasticity of the different layers inside cuticle scales. These scientists showed that the scales of Asian hair are re- moved faster by wet sonication after extension to 35% or by bleaching the hair followed by shampooing and combing the hair over a large number of cycles. In the latter case, after 90 times for four cycles, fewer scales were found on Asian hair relative to Caucasian hair (3.2 vs 1.3 scales, respectively). On further examination of the hair using an atomic force microscopic probe, these scien- tists found a greater difference in elasticity as a function of depth for the Caucasian hair (1.41 vs 1.26), and they concluded that the scales of Asian hair are more uniform inside and that therefore the intracellular matter of Asian hair cuticle is more resistant to frac- turing. Therefore, they concluded that the scales of Asian hair are removed more by frac- turing in the cuticle–cuticle CMC (even in the wet state), while the scales of Caucasian hair fractures inside the scales are most likely in the swollen endocuticle. It is interesting to note here that Nakamura et al. (8) by staining reactions has concluded that the com- position of the proteins of the delta layer of the cuticle–cuticle CMC is very much like that of the very hydrophilic endocuticle. CMC LIPIDS DEGRADED BY VISIBLE LIGHT MORE THAN BY UV Hoting and Zimmerman (88) have studied radiation damage as a function of wavelength and have shown that the CMC lipids of hair fi bers are degraded most by visible light, but also by UV-A and UV-B light, helping to explain the weakened CMC (of cuticle and cortex) and the multiple-step fractures that result from the axial propagation of cracks through the cortex–cortex CMC in sunlight-oxidized hair. Obvious weak links to photochemical attack on lipid structures are the tertiary hydrogen atoms of 18-methyl eicosanoic acid (89) and cholesterol and cholesterol sulfate. The allylic hydrogen atoms of oleic and palmitoleic acids and of cholesterol and cholesterol sulfate in the cortex–cortex CMC are also vulnerable to photo-oxidative reactions. Long-term irradiation does not provide for clean breakage between structural compo- nents of human hair, as was observed for peroxide-oxidized hair, but leads to cross-linking

JOURNAL OF COSMETIC SCIENCE 460 or fusion reactions similar to long-term irradiation effects on wool fi ber, as explained in the next section of this review (90). For hair damaged by sunlight, in most cases, the lipids of the cuticle–cuticle CMC sometimes appear altered to a greater extent than the more susceptible areas of the cortex–cortex CMC because the outer layers of the fi ber re- ceive higher intensities of radiation. SHORT-TERM IRRADIATION ATTACKS CMC LIPIDS, PRODUCING INTERNAL STEP FRACTURES Fracturing of wool fi ber exposed to simulated sunlight has been studied microscopically by Zimmermann and Hocker (90). Electron micrographs of human hair fi bers exposed to simulated sunlight and then fractured, showing that human hair provides similar effects to those of wool fi ber, have been provided to this author by Sigrid Ruetsch. Zimmerman and Hocker demonstrated that stretching nonirradiated control wool fi bers in water provided primarily smooth fractures, while short and intermediate times of simulated sunlight exposure caused the fi bers to break mainly as step fractures. These scientists suggested that short- and intermediate-term irradiation damages the lipids of the CMC (all three types of CMC) and thereby provides many internal step-type fractures by axial propagation of cracks through the photochemically damaged cortex–cortex CMC. Longer-term irradiation creates crosslinks in the hair, fusing it and creating amorphous fractures. Thus, short- and intermediate-term irradiation attacks CMC lipids, providing for in- creased beta-delta failure in the cuticle–cuticle CMC and multiple step fractures in the cortex–cortex CMC. Longer-term irradiation produces amorphous fractures by fusion re- actions through the creation of carbonyl groups that are cross-linked through lysine groups, analogous to the oxidative damage to proteins and mitochondrial decay associ- ated with aging, as described by Dean et al. (91). These fusion reactions start in the pe- riphery of the fi ber, where it receives higher intensities of radiation than the core, providing a smooth fracture at the periphery and multiple step fractures in the interior of the fi bers and, if exposed long enough to light radiation, amorphous fractures are pro- duced across the entire fi ber. Short- and intermediate-term exposures to radiation are propagated by abstraction of hydrogen atoms from tertiary carbon atoms of 18-MEA (89) and of allylic hydrogen at- oms of oleic and palmitoleic acids in free lipids of the cuticle–cuticle CMC. The cortex– cortex CMC contains tertiary hydrogen atoms on cholesterol and cholesterol sulfate and allylic hydrogen atoms on oleic and palmitoleic acids, and on cholesterol and cholesterol sulfate, which react similarly. The abstraction of hydrogen atoms from tertiary carbon atoms on amino acid side chains (analogous to the tertiary carbon atoms on 18-MEA and cholesterols) has been shown by Goshe et al. (92) to predominate over the abstraction of hydrogen atoms at the alpha carbon atom of amino acids in polypeptides. This fact helps to explain why the beta layers are degraded faster by photo-oxidation than the hair proteins via the cross-linking fusion reactions and why step fractures are produced on short- and intermediate-term radiation exposures, while amorphous fractures are produced only after longer-term exposures. Hoting and Zimmermann (88) have also demonstrated that the CMC lipids of the cortex of hair, previously bleached with peroxide-persulfate, are more readily degraded by radiation