Premalatha B, Sachdanandam P
Department of Medical Biochemistry, Dr. A.L.M. Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, 600 113, India.
Pharmacol Res. 2000 Jan;41(1):19-24. doi: 10.1006/phrs.1999.0544.
As part of a substantial effort to curtail the adverse health effects posed by aflatoxin B(1), studies have been conducted to elucidate the possible mechanism for the anticarcinogenic action of Semecarpus anacardium nut extract against aflatoxin B(1)-induced hepatocellular carcinoma. Rats are monitored for levels of urinary, serum and liver biomarkers, namely, unmetabolised aflatoxin B(1), and its metabolites aflatoxin M(1), and aflatoxin Q(1), over the course of 2 weeks with nut extract therapy following a single-exposure to aflatoxin B(1). Due to the administration of nut extract, the excretion of unmetabolised aflatoxin B(1) was increased in day 1 urine when compared with rats without drug treatment. In serum and liver which were collected on day 16 and the rest of periodical urine samples showed aflatoxin B(1) and its metabolites in undetectable levels. The nut extract administration induced cytochrome P(450), glutathione, and glutathione-S-transferase levels in liver homogenates of aflatoxin B(1)-treated rats. These data seem to indicate that anticarcinogenic action by Semecarpus anacardium nut extract is possibly via suppression of aflatoxin B(1)activation and through interaction with microsomal-activating components. Previous evidence from this laboratory about the potency of Semecarpus anacardium nut extract against aflatoxin B(1)-induced hepatocellular carcinoma together with the present results suggest that extremely effective therapeutic protection can be achieved by this drug against aflatoxin B(1)-mediated ill effects.
作为减少黄曲霉毒素B(1)对健康产生不良影响的一项重要工作的一部分,已开展研究以阐明印度没药坚果提取物对黄曲霉毒素B(1)诱导的肝细胞癌的抗癌作用可能的机制。在单次接触黄曲霉毒素B(1)后,用坚果提取物进行为期2周的治疗,在此期间监测大鼠尿液、血清和肝脏生物标志物的水平,即未代谢的黄曲霉毒素B(1)及其代谢产物黄曲霉毒素M(1)和黄曲霉毒素Q(1)。由于给予了坚果提取物,与未接受药物治疗的大鼠相比,第1天尿液中未代谢的黄曲霉毒素B(1)的排泄量增加。在第16天采集的血清和肝脏以及其余定期尿液样本中,黄曲霉毒素B(1)及其代谢产物的水平均未检测到。给予坚果提取物可诱导黄曲霉毒素B(1)处理的大鼠肝脏匀浆中的细胞色素P(450)、谷胱甘肽和谷胱甘肽-S-转移酶水平。这些数据似乎表明,印度没药坚果提取物的抗癌作用可能是通过抑制黄曲霉毒素B(1)的活化以及与微粒体活化成分相互作用来实现的。该实验室先前关于印度没药坚果提取物对黄曲霉毒素B(1)诱导的肝细胞癌的效力的证据以及目前的结果表明,这种药物可对黄曲霉毒素B(1)介导的不良影响实现极其有效的治疗性保护。