Hasan S S, Joshi A
School of Sciences, Indira Gandhi National Open University, Maidan Garhi, New Delhi, India.
Radiol Med. 1994 Jun;87(6):837-46.
The role of AMP was investigated in radiosensitization by the use of prochlorperazine in normal rat skin. AMP metabolism was evaluated by estimating the level of activities of 5' nucleotidase vis-à-vis protein, DNA and RNA contents in prochlorperazine-treated plus irradiated skin. To study radiation-induced changes in the skin, the extent of lipid peroxidation was measured in terms of enzyme lipid peroxidase. After irradiation, lipid peroxidase activity was observed to increase in prochlorperazine-treated rat skin. Subsequently the level of 5' nucleotidase was found to decrease in drug-treated plus irradiation skin. Similarly, the suppression in the levels of DNA, RNA and protein contents increased when the rat skins was irradiated in the presence of sensitizer prochlorperazine. The cytological examination, which revealed the extent of the lesions occurring in the normal rat skin, and the biochemical examination demonstrated increased cellular lethality in prochlorperazine-sensitized skin after irradiation. The results suggest that prochlorperazine probably sensitizes the normal skin tissues to radiation by inhibiting AMP metabolism via hydroxy-radical-induced decrease in DNA, RNA and protein metabolism.
通过在正常大鼠皮肤中使用氯丙嗪来研究腺苷一磷酸（AMP）在放射增敏中的作用。通过评估氯丙嗪处理加照射皮肤中5'核苷酸酶活性水平相对于蛋白质、DNA和RNA含量来评价AMP代谢。为了研究皮肤中辐射诱导的变化，以脂质过氧化物酶为指标测量脂质过氧化程度。照射后，观察到氯丙嗪处理的大鼠皮肤中脂质过氧化物酶活性增加。随后发现，药物处理加照射皮肤中5'核苷酸酶水平降低。同样，当大鼠皮肤在增敏剂氯丙嗪存在下接受照射时，DNA、RNA和蛋白质含量的抑制作用增强。细胞学检查揭示了正常大鼠皮肤中发生的损伤程度，生化检查表明照射后氯丙嗪增敏皮肤中的细胞致死率增加。结果表明，氯丙嗪可能通过羟基自由基诱导的DNA、RNA和蛋白质代谢减少来抑制AMP代谢，从而使正常皮肤组织对辐射敏感。
