No abstract

Changes in clinical pathology parameters, particularly those related to blood coagulation, were examined throughout the gestation period in New Zealand White rabbits. As compared with the non-pregnant group, the following major changes were observed in the pregnant group. For blood coagulation-related parameters, platelets increased progressively and fibrinogen increased slightly from organogenesis, prothrombin time was significantly prolonged during organogenesis and shortened in the late fetal growth stage, activated partial thromboplastin time was significantly prolonged during the fetal growth stage, and antithrombin III increased during and after late organogenesis. Such changes in blood coagulation-related parameters during the later stages of gestation seem to be physiological responses in preparation for protecting against excessive haemorrhage or haemostasis at parturition. For the other haematological and blood chemical parameters as well as progesterone, red blood cell counts, haemoglobin and haematocrit began to decrease during organogenesis and continued to decrease thereafter. Reticulocyte counts significantly increased during organogenesis and decreased thereafter. White blood cell parameters, except for neutrophils, showed significant decreases during the fetal growth stage. Serum progesterone concentration reached its highest level early in organogenesis and decreased thereafter. Total protein, albumin, glucose, cholesterol, calcium, blood urea nitrogen and creatinine decreased significantly during the middle and/or late periods of gestation. In conclusion, the data obtained from the present study can be used as background data for effective evaluation of reproductive toxicology in rabbits, and pregnant rabbits may serve as models of pregnant women in research pertaining to clinical pathology and gestation.

No abstract

-This study's aim is to investigate the relationship between stage and degree of restricted feeding during the gestation period and occurrence of abortion, premature birth or fetal damage in rabbits. The study was composed of 5 groups of pregnant Kbl:NZW rabbits that consisted of 8 animals each. These groups were subjected to restricted feeding in the following ways: (A) control group, free access to food, (B) 60 g per day from gestational days (GD) 6 to 18 (middle period), (C) 20 g per day from GD 6 to 18, (D) 20 g per day from GD 19 to 28 (post-middle period), and (E) 20 g per day from GD 6 to 28 (middle and post-middle periods). Even though all dams in Groups A, B and C went to full term, abortion or premature birth occurred to 2/8 and 8/8 dams in Groups D and E, respectively. Fetal lethality increased in Group C, which was subjected to restricted feeding at 20 g/head/day in the middle period. Slight inhibition of fetal growth was recorded only in Group D, which was subjected to restricted feeding in the postmiddle period. Restricted feeding at 20 g/head/day in the middle period induced no abortion or premature birth, but increased fetal lethality that in the middle and post-middle periods resulted in abortion or premature birth of all dams, and that in the post-middle period resulted in abortion or premature birth at low incidence and slightly inhibited fetal growth. These results demonstrated that the post-middle period is vulnerable to effects of reduced food consumption in pregnant rabbits.

No abstract

The effects of 1‐O‐hexyl‐2,3,5‐trimethylhydroquinone (HTHQ), phenylethyl isothiocyanate (PEITC), 3‐O‐ethylascorbic acid, 3‐O‐dodecylcarbomethylascorbic acid and n‐heptadecane‐8,10‐dione were analyzed in a rat multiorgan carcinogenesis model. Groups of 15 animals were given a single intraperitoneal (i.p.) injection of diethylnitrosamine and 4 i.p. injections of N‐methylnitrosourea as well as N‐butyl‐N‐(4‐hydroxybutyl)nitrosamine in the drinking water during the first 2 weeks. Then 4 subcutaneous (s.c.) injections of dimethylhydrazine and 2,2′‐dihydroxy‐di‐n‐propylnitrosamine were given in the drinking water over the next 2 weeks for initiation. Test compounds were administered during the initiation or post‐initiation periods. The dietary dose was 1% except for n‐heptadecane‐8,10‐dione and PEITC (0.1%). Complete autopsy was performed at the end of experimental week 28. All 5 compounds reduced the number of lung hyperplasia, particularly PEITC when given during the initiation period. In addition, HTHQ lowered the incidence of esophageal hyperplasia in the initiation period, and of small and large intestinal adenomas in the post‐initiation period. However, it also enhanced the development of hyperplasia and papilloma in the forestomach and tongue. PEITC lowered the induction of esophageal hyperplasia, kidney atypical tubules and liver glutathione S‐transferase placental form (GST‐P)‐positive foci when given during the initiation period but enhanced the development of liver GST‐P positive foci and urinary bladder tumors in the post‐initiation period. Moreover, it induced hyperplasia of the urinary bladder. Our results indicate minor adverse effects for HTHQ in the forestomach and tongue, and demonstrate that PEITC, which inhibits carcinogenesis at the initiation stage in several organs, also exhibits promotion potential in liver and urinary bladder in the post‐initiation stage under the present experimental conditions. Int. J. Cancer 76:851–856, 1998.© 1998 Wiley‐Liss, Inc.

No abstract

The effects of 1-O-hexyl-2,3,5-trimethylhydroquinone (HTHQ), phenylethyl isothiocyanate (PEITC), 3-O-ethylascorbic acid, 3-O-dodecylcarbomethylascorbic acid and n-heptadecane-8,10-dione were analyzed in a rat multiorgan carcinogenesis model. Groups of 15 animals were given a single intraperitoneal (i.p.) injection of diethylnitrosamine and 4 i.p. injections of N-methylnitrosourea as well as N-butyl-N-(4-hydroxybutyl)nitrosamine in the drinking water during the first 2 weeks. Then 4 subcutaneous (s.c.) injections of dimethylhydrazine and 2,2Ј-dihydroxy-di-n-propylnitrosamine were given in the drinking water over the next 2 weeks for initiation. Test compounds were administered during the initiation or post-initiation periods. The dietary dose was 1% except for n-heptadecane-8,10-dione and PEITC (0.1%). Complete autopsy was performed at the end of experimental week 28. All 5 compounds reduced the number of lung hyperplasia, particularly PEITC when given during the initiation period. In addition, HTHQ lowered the incidence of esophageal hyperplasia in the initiation period, and of small and large intestinal adenomas in the post-initiation period. However, it also enhanced the development of hyperplasia and papilloma in the forestomach and tongue. PEITC lowered the induction of esophageal hyperplasia, kidney atypical tubules and liver glutathione S-transferase placental form (GST-P)-positive foci when given during the initiation period but enhanced the development of liver GST-P positive foci and urinary bladder tumors in the post-initiation period. Moreover, it induced hyperplasia of the urinary bladder. Our results indicate minor adverse effects for HTHQ in the forestomach and tongue, and demonstrate that PEITC, which inhibits carcinogenesis at the initiation stage in several organs, also exhibits promotion potential in liver and urinary bladder in the post-initiation stage under the present experimental conditions. Int.