METHOD: Lifespan was determined by counting the number of surviving nematodes daily under a dissecting microscope after treatment with hydrogen peroxide and the tocotrienol-rich fraction. The evaluated oxidative markers included lipofuscin, which was measured using a fluorescent microscope, and protein carbonyl and 8-hydroxy-2'-deoxyguanosine, which were measured using commercially available kits.
RESULTS: Hydrogen peroxide-induced oxidative stress significantly decreased the mean lifespan of C. elegans, which was restored to that of the control by the tocotrienol-rich fraction when administered before or both before and after the hydrogen peroxide. The accumulation of the age marker lipofuscin, which increased with hydrogen peroxide exposure, was decreased with upon treatment with the tocotrienol-rich fraction (p<0.05). The level of 8-hydroxy-2'-deoxyguanosine significantly increased in the hydrogen peroxide-induced group relative to the control. Treatment with the tocotrienol-rich fraction before or after hydrogen peroxide induction also increased the level of 8-hydroxy-2'-deoxyguanosine relative to the control. However, neither hydrogen peroxide nor the tocotrienol-rich fraction treatment affected the protein carbonyl content of the nematodes.
CONCLUSION: The tocotrienol-rich fraction restored the lifespan of oxidative stress-induced C. elegans and reduced the accumulation of lipofuscin but did not affect protein damage. In addition, DNA oxidation was increased.
METHODS: This was a prospective, cross sectional study recruiting injured motorcyclists from Hanoi, Vietnam hospital. The participants were interviewed by a trained researcher. The participants' helmets were collected post-crash. Initially, the helmets were examined for their type and external characteristics. A 3 cm × 3 cm cut was made on the helmet in the impacted and non-impacted areas (control). These areas were investigated for evidence of POD and presence of micro-cracks and material disintegration. 50 participants were enrolled. Sources of information included questionnaire and laboratory analyses. The helmet factors of interest were age of the helmet, exposure of helmet to sunlight and rain (duration/day) and history of previous impact. Laboratory analyses included Fourier Transform Infra Red (FTIR) for degradation and scanning electron microscopy (SEM) for micro-structural examination.
RESULTS: Majority of the helmets was the open-face type, 40 (80.0%). 31 (62.0%) helmets aged less than three years (LTY) and 19 (38.0%) were three years old or more (MTY). 19 (61.3%) of the LTY helmets and 12 (63.2%) MTY helmets showed evidence of POD. The duration of helmet exposure to sunlight was between 93 to 6570 hours (mean 2347.74 hours; SD 1733.39). The SEM showed 15 helmets (30%) with micro-fractures, 21 helmets (42.0%) with material disintegration. Prolonged uv exposure to the ABS helmets resulted in changes in the helmet material in the form of material disintegration and microcracks and this association was statistically significant (p = 0.03).
CONCLUSION: POD occurs due to routine exposure to the ultraviolet light. Prolonged uv exposure affects outer shell surface material integrity.