Figure 8: Chronic ethanol exposure and PPAR agonist treatment effects on RER structure. Adult male Long Evans rats were fed with liquid diets containing (A-D) 0% or (E-H) 37% ethanol for 8 weeks, and administered i.p. injections of (A,E) vehicle, or a (B,F) PPAR-α, (C,G) PPAR- δ, or (D,H) PPAR-γ agonist. Spurr’s resin-embedded, 50-60 nm thick sections of liver sections were contrasted with uranyl acetate and lead citrate and examined by EM. (AD) Control livers had relatively uniform parallel stacks of flattened RER cisternae with regularly spaced ribosomes. PPAR-α agonist treatments resulted in patchy absence of ribosomes (arrowheads) on the ER in both (B) control and (F) ethanol-exposed livers. (E) Ethanol+vehicle treated livers had disrupted, disorganized RER. This phenomenon was prevented by (F-H) PPAR agonist treatment. However, in ethanol-exposed livers, the RER cisternae were variably dilated and irregularly populated by ribosomes. Original magnification, 71000x.