Study on the regulation of autophagy against anticancer drugs' toxicity / 药学学报

Autophagy is a crucial biological process in eukaryotes, which is involved in cell growth, survival and energy metabolism. It has been confirmed that autophagy mediates toxicity of anticancer drugs, especially in heart, liver and neuron. It is important to understand the function and mechanism of autophagy in anticancer drugs-induced toxicity. Given that autophagy is a double-edged sword in the maintenance of the function of heart, liver and neuron, the autophagy-mediated toxicity are very complicated in the body. We provide a review on the concept of autophagy and current status about autophagy-mediated toxicity of anticancer drugs. The knowledge is crucial in the basic study of anticancer drugs-induced toxicity, and provides some strategies for the development of alleviating the toxicity of anticancer drugs.

Study on the regulation of autophagy against anticancer drugs' toxicity / 药学学报

Autophagy is a crucial biological process in eukaryotes, which is involved in cell growth, survival and energy metabolism. It has been confirmed that autophagy mediates toxicity of anticancer drugs, especially in heart, liver and neuron. It is important to understand the function and mechanism of autophagy in anticancer drugs-induced toxicity. Given that autophagy is a double-edged sword in the maintenance of the function of heart, liver and neuron, the autophagy-mediated toxicity are very complicated in the body. We provide a review on the concept of autophagy and current status about autophagy-mediated toxicity of anticancer drugs. The knowledge is crucial in the basic study of anticancer drugs-induced toxicity, and provides some strategies for the development of alleviating the toxicity of anticancer drugs.

Research progress in toxicology of molecular targeted anticancer drugs / 浙江大学学报·医学版

Drug therapy is essential for cancer treatment. The molecular targeted anticancer drugs develop rapidly in recent years, since the effectiveness of traditional chemotherapy is unsatisfactory and the adverse reactions are high. However, molecular targeted anticancer drugs would damage the function of heart, liver or lung, and may cause adverse effects such as hand-foot syndrome, which restrains their clinical application. Therefore, it is critical for pharmaceutical toxicology to study the toxicity, the related mechanisms and the preventive measures of molecular targeted anticancer drugs.

Lipid-peroxidantion damage of embryo and placenta induced by artesunate in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To examine the effect and mechanism of artesunate (Art) on embryo development.</p><p><b>METHODS</b>Rat embryo and placental glutathione peroxidase (GSH-Px)and malondialdehyde (MDA) were identified by using DTNB (dithionitrobenzene) direct method and TBA (thiobarbituric acid). We investigated the damage of decidual cells caused by Art using cell culture techniques.</p><p><b>RESULTS</b>Subcutaneous administration of Art in rats on d 6 approximate, equals d 10 of gestation induced developmental toxicity. Absorption increased when progressively increased doses were given (r=0.996,P<0.01). Twenty four hours post injection, GSH-Px in embryo decreased significantly while MDA content was significantly higher than that in the control group (P<0.05). GSH Px: study group was(43.7+/-10.7)micromol/min.mg(-1)Hb, control group was(54.5+/-10.1)micromol/min.mg(-1)Hb; MDA:study group was(230.2+/-19.8)nmol/g tissue, control group was(150.4+/-44.1)nmol/g tissue. Placental GSH-Px activity was significantly higher than that in the control group(P<0.01). After cultured human decidual cells were exposed to Art for 24 h, the LC50 was (25.2+/-3.5)mg/L.</p><p><b>CONCLUSION</b>Art may induce developmental toxicity in rat embryo and placenta by neutralizing the antioxidant defense mechanism.</p>