[
Clinics (Sao Paulo),
2013]
OBJECTIVE: This study was performed to determine the effect of the tocotrienol-rich fraction on the lifespan and oxidative status of C. elegans under oxidative stress. 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.
[
Development,
1987]
Most nematodes have XO male/XX female sex determination. C. elegans is anomalous, having XX hermaphrodites rather than females. The hermaphrodite condition appears to result from the modification of a basic male/female sex-determination system, which permits both spermatogenesis and oogenesis to occur within a female soma. This modification is achieved by a germ-line-specific control acting at one step in a cascade of autosomal regulatory genes, which respond to X-chromosome dosage and direct male, female, or hermaphrodite development. Mutations of one of these genes can be used to construct artificial strains with ZZ male/WZ female sex determination. Primary sex determination normally depends on the ratio of X chromosomes to autosomes, as in Drosophila, and there appear to be multiple sites on the X chromosome that contribute to this ratio. Also, as in Drosophila, X-chromosome expression is compensated to equalize gene activity in XX and XO animals. Interactions between dosage compensation and sex determination are described and discussed.