The cyclopropene fatty acids, sterculic and malvalic, occur
naturally in a major food lipid, cottonseed oil, and have been implicated
in several physiological disorders. Rainbow trout in this
study were fed semipurified diets containing 200 or 300 ppm methyl
sterculate, and the effects on hepatic lipid and glycogen levels,
lipid incorporation of radioactive phosphate and fatty acids, and
mitochondrial energy production were investigated.
Chronic ingestion of methyl sterculate caused numerous histological
changes and some necrosis in the liver. Glycogen accumulated
in irregular pockets, but the level in whole liver was not
increased over controls. Hepatic lipid accumulation was noted after
several weeks, reaching a level six times that of controls after six
months. Liver weight of the sterculate-fed fish decreased in proportion to body weight during the first three weeks on the sterculate
diet, but after three months became significantly greater than
controls.
Ingestion of 200 ppm methyl sterculate for two weeks by trout
caused reduced incorporation of both phosphate and fatty acids into
phospholipids. The major reductions were found in minor fractions.
Label incorporation into cardiolipin, important for mitochondrial
function, was reduced ten-fold by the dietary sterculate. Incorporation
into a minor unknown phospholipid which constituted less than
1% of total phospholipids was reduced as much as 135-fold in the
mitochondrial fraction. Incorporation of 1-¹⁴C-oleate into diglycerides
was also inhibited.
The major changes caused by methyl sterculate appear to occur
in mitochondria. Neither the level of cytochrome P⁴⁵⁰ nor the
activity of NADPH neotetrazolium reductase, both of which occur in
the endoplasmic reticulum, was altered. P/0 ratios and the ability
to oxidize oleic acid to CO₂ were curtailed after only two weeks on
a diet containing methyl sterculate
