Rh2 is a ginsenoside extracted from ginseng that has drawn attention in a few laboratories in Asian countries because of its potential tumor-inhibitory effect. In the present study, we tested Rh2 on many tumor-cell lines for its effects on cell proliferation, induction of apoptosis, and potential interaction with conventional chemotherapy agents. Our results showed that Rh2 inhibited cell growth by G1 arrest at low concentrations and induced apoptosis at high concentrations in a variety of tumor-cell lines, possibly through activation of caspases. The growth arrest and apoptosis may be mediated by 2 separate mechanisms. Apoptosis is not dependent on expression of the wild-type p53 nor the caspase 3. In addition, the apoptosis induced by Rh2 was mediated through glucocorticoid receptors. Most interestingly, Rh2 can act either additively or synergistically with chemotherapy drugs on cancer cells. Particularly, it hypersensitized multidrug-resistant breast cancer cells to paclitaxel. These results suggest that Rh2 possesses strong tumor-inhibiting properties, and potentially can be used in treatments for multidrug-resistant cancers, especially when it is used in combination with conventional chemotherapy agents.

Different liquid diets were tested as vehicles for ethanol administration in order to maximize the blood ethanol level (BEL) in rats. This was done since maternal BEL during the gestation period is believed to be the determining factor for behavioral and neurochemical changes in the offspring. A comparative study with three different liquid diets indicated that the Sustacal and Lieber-DeCarli diets were more effective in elevating the BEL than the Bio-Mix diet. Furthermore, it was observed that prenatal ethanol exposure affected to a varying extent the neuromuscular abilities (detected by rotarod test) and maze-learning in the offspring of mothers that receive ethanol through Lieber-DeCarli diet. No significant (P < 0.01) behavioral changes were observed in the offspring of mothers that received the Bio-Mix diet containing ethanol.Key words: fetal alcohol syndrome (FAS), blood ethanol level (BEL), animal models of FAS, alcohol teratogenicity, behavioral teratology