1[1]Geoffrion Y, Rydzy M. The use of immobilized ferrite to enhance the depth selectivity of in vivo surface coil NMR spectroscopy [J] . NMR Biomed, 1988,1(3) :107 - 112.
2[2]Jehenson P. Correction for the contamination by muscle signal of in vivo 31P-NMR spectra of the liver and kidney [J] . J Magn Resonance, 1992,96:181 - 184.
3[3]Malloy CR, Cunningham CC, Radda GK, et al. The metabolic state of the rat liver in vivo measured by31 P-NMR spectroscopy [J]. Biochim Biophys Acta, 1986,885:1 - 11.
4[4]Berson A, Renault S, Letteron P, et al. Uncoupling of rat and human mitochondria: a possible explanation for tacrineinduced liver dysfunction [J]. Gastroenterlogy, 1996,110:1878 - 1890.
5[5]Watanabe H, Kobayashi A, Yamamoto T, et al. Alterations of human erythrocyte membrane fluidity by oxygen-derived free radicals and calcium [J]. Fre Rad Biol Med, 1990,8:507 - 511.
6[6]Parmar DV, Ahmed G, Khandkar MA, et al. Mitochondrial ATPase: a target for paracetamol-induced hepatotoxicity [J].Eur J Pharmacol, 1995,293: 225 - 229.
7[7]Takahashi H, Geoffrion Y, Butler K, et al. In vivo hepatic energy metabolism during the progression of alcoholic liver diseases: a noninvasive 31P NMR study in rats [J]. Hepatology, 1990,11(1) :65 - 73.
8[8]Meyers LL, Beierschmitt WP, Khairallah EA, et al. Acetaminophen-induced inhibition of hepatic mitochondrial respiration in mice [J]. Toxicol App Pharamcol, 1988,93:378 - 388.
9[9]Katyare SS, Satav JG. Impaired mitoehondrial oxidative energy metabolism following paracetamol-induced hepatotoxicity in the rat [J]. Br J Pharmacol, 1989,96:51- 58.
