The effects of luteinizing hormone (LH) and human chorionic gonadotrophic hormone (hCG) on Leydig cell structure and function are reviewed in this paper under two main headings; responses to LH and hCG stimulation and responses to LH deprivation. With acute LH stimulation, up to 2 hours following the LH injection, there was no change in the volume of a Leydig cell. However, Leydig cell peroxisomal volume and intraperoxisomal SCP2 content showed a rapid and transient change. These changes can be considered to be specific because: i) no other Leydig cell organelle including smooth endoplasmic reticulum (SER) showed such a change, and ii) only the intraperoxisomal SCP2 but not catalase (a marker enzyme for peroxisomes) showed such a change within 30 minutes of LH stimulation. As these changes occurred prior to the peak testosterone levels following this treatment, it is suggested that SCP2 and peroxisomes may have an association with testosterone biosynthesis prior to cholesterol transport into mitochondria. With LH or hCG stimulation for longer periods, i.e. one day or more, the same morphological changes are produced in Leydig cells irrespective of the age of the species, dosage of LH or hCG, and with single or multiple doses. These changes include, Leydig cells hypertrophy and/or hyperplasia, increase in the cellular organelle content (mostly SER and mitochondria) and depletion of lipid droplets. In addition, a recent study showed that Leydig cell peroxisomal volume, SCP2 content, the amount of intraperoxisomal SCP2 and testosterone secretory capacity were also significantly increased in response to chronic LH treatment. The effects of LH deprivation by whatever means (e.g. hypophysectomy, with testosterone and 17 beta-estradiol silastic implants, LH antisera) on Leydig cell structure and function is generally described as opposite to those observed following LH or hCG stimulation. These include Leydig cell hypotrophy and hypoplasia, reductions in the cytoplasmic organelle content in general and specific reductions in SER and peroxisomal volumes, reductions in total catalase and SCP2 in Leydig cells together with reductions in the intraperoxisomal SCP2 content in Leydig cells and their testosterone secretory capacity.