Cholesterol utilized for steroid synthesis by ovarian tissue may be derived from de novo synthesis or cellular uptake of lipoprotein cholesterol. The majority of blood cholesterol is transported by either low (LDL) or high (HDL) density lipoproteins, depending on the animal species. Prior to vascularization, only HDL are in follicular fluid and contribute sterol to granulosa cells because other lipoproteins are unable to transverse the basement membrane due to their molecular masses. Following vascularization, both LDL and HDL bathe luteal cells. Most species preferentially use LDL cholesterol as a precursor for ovarian steroid synthesis. The LDL uptake by ovarian tissue occurs by receptor-mediated endocytosis. The receptor recognizes apolipoprotein B of LDL and apolipoprotein E found on some, but not all, HDL. Within a species, a positive relationship may exist between HDL apolipoprotein E content and importance of HDL cholesterol as a precursor for steroidogenesis. A "HDL pathway" exists for uptake of sterol from HDL void of apolipoprotein E. The HDL receptor exhibits broad binding specificity. Unlike LDL, the HDL particle is not internalized, and cholesterol preferentially is taken up relative to other HDL constituents. In most species, lipoproteins, rather than de novo synthesis from acetate, contribute the majority of cholesterol used for steroid production. Trophic hormones increase lipoprotein binding, internalization, degradation and conversion of lipoprotein-derived sterol to steroids, effects that are mediate through cyclic adenosine monophosphate. Knowledge recently acquired regarding lipoprotein sterol utilization by the ovary may be useful in developing nutritional, pharmacological or endocrine manipulations that may positively affect cholesterol clearance by the ovary, steroidogenesis and reproductive performance.