Wainstok de Calmanovici R, Cochón A C, Zenklusen J C, Aldonatti C, Cabral J R, San Martín de Viale L C
Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina.
Cancer Lett. 1991 Jul 4;58(3):225-32. doi: 10.1016/0304-3835(91)90105-q.
The response of female BDVI rats bearing diethylnitrosamine(DENA)-induced hepatic tumors to the porphyrinogenic action of hexachlorobenzene (HCB) was studied. (1) The heme pathway operates in these tumors but they were less affected by HCB than the liver. (2) Tumors did not accumulate porphyrins although the surrounding liver accumulated more porphyrins than livers treated with HCB. (3) DENA/HCB livers which developed a well defined tumor showed slightly less porphyrinogen carboxylyase inhibition and delta-aminolaevulinate synthase induction than HCB rats. (4) The results of the present work suggest that endogenously formed porphyrins would be unable to be accumulated by DENA-induced tumors when the tumoral development precedes the onset of the porphyria.
研究了携带二乙基亚硝胺(DENA)诱导的肝肿瘤的雌性BDVI大鼠对六氯苯(HCB)致卟啉生成作用的反应。(1)血红素途径在这些肿瘤中起作用,但它们受HCB的影响小于肝脏。(2)肿瘤不积累卟啉,尽管周围肝脏比用HCB处理的肝脏积累更多的卟啉。(3)形成明确肿瘤的DENA/HCB肝脏显示出比HCB大鼠略少的卟啉原羧化酶抑制和δ-氨基乙酰丙酸合酶诱导。(4)本研究结果表明,当肿瘤发展先于卟啉病发作时,内源性形成的卟啉将无法被DENA诱导的肿瘤积累。