Srivastava P, Puri S K, Pandey V C
Biochemistry Division, Central Drug Research Institute, Lucknow, India.
Int J Parasitol. 1994 Aug;24(5):677-9. doi: 10.1016/0020-7519(94)90120-1.
Plasmodium berghei infection impaired the hepatic heme synthesizing machinery of mice. Key enzymes, viz. S-aminolevulinic acid synthase, S-aminolevulinic acid dehydrase and ferrochelatase were found to be decreased. In contrast, tryptophane pyrrolase noticeably increased during parasitic infection. Oral feeding of chloroquine [16 mg (kg body weight)-1 x 4 days] cleared the parasitaemia from infected mice within 72 h and returned the altered levels of enzymes almost to normal a week after cessation of treatment, the exception being tryptophane pyrrolase, which remained unaffected. Chloroquine treatment did not cause any significant alteration in the above-mentioned enzymes of normal mice.
伯氏疟原虫感染损害了小鼠肝脏的血红素合成机制。关键酶，即δ-氨基乙酰丙酸合成酶、δ-氨基乙酰丙酸脱水酶和亚铁螯合酶的水平均下降。相比之下，色氨酸吡咯酶在寄生虫感染期间显著增加。口服氯喹[16毫克/（千克体重）-1×4天]可在72小时内清除感染小鼠的寄生虫血症，并在治疗停止一周后使改变的酶水平几乎恢复正常，但色氨酸吡咯酶除外，其水平未受影响。氯喹治疗对正常小鼠的上述酶没有引起任何显著改变。
