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Aim To compare acute toxicity of Liu-Shen-Wan (LSW), realgar, Chan-Su, and sodium arsenate in mice. Method Mice were given orally LSW, realgar, arsenate (As5+), and Chan-Su. Acute toxicity and tissue As accumulation were determined 8 hrs later.Results As5+ increased alanine aminotransferase (ALT) and blood urea nitrogen (UREA) levels, indicative of liver and kidney injury. No elevation of ALT and UREA was observed in LSW, realgar and Chan-Su groups. Histopathology showed more lesions in As5+ -treated liver, kidney and heart, while these lesions were mild or absent in Chan-Su, realgar and LSW groups,In Chan-Su-treated heart, cardiac lesions were observed, but were less severe as compared to As5+. As5+ administration resulted in As accumulation in liver (3560 ng·g-1), kidney (4570 ng·g-1) and heart (410 ng·g-1), much higher than that after LSW (260,180 and 160 ng·g-1). Metallothionein expression was dramatically induced by As5+ in liver (14x), kindey (25x), and heart (180x), but was basically unchanged after LWS, realgar and Chan-Su. Conclusions LSW and realgar are much less toxic acutely than As5+, and the use of total As content to evaluate LSW safety appear to be inappropriate. Objective To examine the effect of Liu-Shen-Wan (LSW) on the proliferation of the human hepatocellular carcinoma Hep3B cells and the potential mechanisms. Methods The proliferative effects of Hep3B cells were determined by the MTS assay. The cell cycle was examined by flow cytometry. The expression of related genes was detected by real-time RT-PCR. Arsenic (As) concentration in cells was examined by Atomic Absorption Spectrometry. Results The proliferation of Hep3B cells for 48 h was suppressed significantly by LSW and NaAs2O3. Cellular As contents in LSW group were higher than other group treated with AS4S4, but were much lower than As3+, As5+ and ATO. LSW induced apoptosis of the cells as evidenced by flow cytometry,and increased expression of BAD. Conclusion LSW was effective in the growth inhibition of the human hepatic carcinoma Hep3B cells. The mechanisms appeared to be related to increased cellular As contents and increased tumor cell apoptosis by regulating gene expressions.
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