Open AccessEffects of Alkyl Alcohols and Related Chemicals on Rat Liver Structure and Function
Author(s) -
Adachi Kayo,
Wakabayashi Takashi,
Popinigis Jerzy
Publication year - 1991
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1991.tb03208.x
Subject(s) - mitochondrion , ethanol , chemistry , alkyl , alcohol , cytochrome c oxidase , cytochrome , biochemistry , hepatocyte , respiratory system , medicine , endocrinology , biology , organic chemistry , enzyme , in vitro
Functional changes of mitochondria in the liver obtained from rats given 32% ethanol, 32% propanol and 6.9% butanol in drinking water for up to 3 months were investigated. Animals were also fed a liquid diet containing ethanol for comparison. Results obtained were as follows: 1) Animals given ethanol in drinking water consumed twice as much ethanol daily as those fed a liquid diet containing ethanol, while ultrastructural changes of hepatic mitochondria were essentially the same between the former and the latter animals: the co‐existence of mega‐mitochondria and small mitochondria with poorly developed cristae. 2) Effects of alkyl alcohols tested on the respiratory rates and coupling efficiency of mitochondria were variable, depending on the kind of alkyl alcohols, the duration of experiments and oxidizable substrates used. 3) There was essentially no difference between the heavy and the light mitochondrial fractions obtained from alkyl alcohol‐treated rat livers in terms of respiratory rates and coupling efficiencies. 4) Decreases in the content of cytochrome aa 3 and the activity of cytochrome oxidase, and increases in MEOS activity were most distinct in ethanol treated rat livers. A possible role of chronic relative oxygen deficiency inside the hepatocyte caused by the metabolization of alkyl alcohols is discussed in order to interpret such peculiar ultrastructural changes of mitochondria. Acta Pathol Jpn 41: 414–427, 1991.