Induction of superovulation in mature mice and rats using serum of spayed female dogs.

The following experiments were designed to examine the effect of serum of spayed dogs on superovulation response in mice and rats. In Experiment 1, female mice at diestrus (n=30) were divided into three equal groups and superovulated with either administration of 5 IU pregnant mare serum gonadotropin (PMSG) or recombinant follicle stimulating hormone (rFSH) (reducing dose from 2.5 to 0.5 IU) and 5 IU human chorionic gonadotropin (hCG) administered 48h later. Serum of spayed dogs was administered intraperitoneally at a reduced dose from 0.1 to 0.025 mL in a 48 h period. In Experiment 2, female rats (n=30) at diestrus stage were divided into three equal groups. Superovulation was induced using either 30 IU PMSG, or a dose reduced from 5 to 1 IU rFSH and 25 IU hCG administered 48h later. Serum of spayed dogs was administered in a reduced dose from 0.6 to 0.1 mL in a 48 hour period. Female mice and rats were mated 24 h following hCG administration. On day 14 after mating, animals were euthanized and ovarian sections were fixed for histopathological evaluation and corpus luteum (CL) counting. No significant difference observed in mean (±SEM) number of CLs between the PMSG group and the mice that received serum of spayed dog (10.4±1.3 vs 9.2±1.0). Mean (±SEM) number of CLs tended to be lower in rats that received serum of spayed dog than those of rats which received either PMSG or rFSH (15.1±1.9 vs 23.6±3.1 and 23.1±2.9, P=0.06, respectively). In conclusion, serum of spayed dogs is able to induce a superovulatory response in mice and rats.

Increased levels of mitochondrial DNA copy number in patients with vitiligo.

BACKGROUND: Oxidative stress is known to be involved in the pathogenesis of autoimmune diseases such as vitiligo. Evidence suggests that the human mitochondrial DNA copy number (mtDNAcn) is vulnerable to damage mediated by oxidative stress. The purpose of this study was to examine and compare peripheral blood mtDNAcn and oxidative DNA damage byproducts (8-hydroxy-2-deoxyguanosine; 8-OHdG) in patients with vitiligo and healthy controls (HCs). METHODS: The relative mtDNAcn and the oxidative damage (formation of 8-OHdG in mtDNA) of each sample were determined by real-time quantitative PCR. Blood samples were obtained from 56 patients with vitiligo and 46 HCs. RESULTS: The mean mtDNAcn and the degree of mtDNA damage were higher in patients with vitiligo than in HCs. CONCLUSION: These data suggest that increase in mtDNAcn and oxidative DNA damage may be involved in the pathogenesis of vitiligo.