Various hormones have been implicated in the process of liver regeneration. Despite the demonstration of specific estrogen receptors (ER) in mammalian liver and the identification of responses to estrogen which occur in liver, there has been little or no investigation of the relation of that hormone or its receptor to liver regeneration or liver growth. Information is provided which indicates the effect of 17.beta.-estradiol on the mass of both intact and regenerating rat liver; the percentage of hepatocytes in neonatal and adult normal intact livers which contain ER, i.e., the estrogen receptor index (ERI); changes in ERI and nuclear ER occurring in that cell population following partial hapatectomy and/or 17.beta.-estradiol administration; and the temporal relation of the changes in ER with those related to DNA synthesis and liver regeneration and to liver growth. Approximately 55-60% of parenchymal cells from intact livers in adult rats contained ER which was entirely located in the cytoplasm. No nuclear ER was evident in such cells. By 1 h, and subsequently following 17.beta.-estradiol administration to such animals, there resulted a depletion in the number of ER-containing cells and the identification of nuclear ER. These changes were followed by the onset of increased DNA synthesis and an increase in liver weight (P < 0.001). Subsequent to 70% PH, a similar series of events occurred in liver remnants. Not only was there a decrease in the ERI from 60% at the time of PH to 40% 3 h later and 30% after 72 h, there was a decrease in cytosol ER as well. Accompanying the decrease was an increase in the number of cells with nuclear ER. By 24 h post-PH, 29% of the cells with ER displayed that receptor in their nuclei. At that time, DNA synthesis was at its peak, and liver regeneration was taking place. When 17.beta.-estradiol was administered at the time of PH, there was a more rapid onset of translocation of ER to the nuclei of parenchymal cells. At PH, when 17.beta.-estradiol was given, no cells displayed nuclear ER. One hour later, 18% of cells with ER had nuclear ER, in contrast to the finding that only 3% of cells had nuclear ER 1 h post-PH when 17.beta.-estradiol was not administered. Regeneration was greater (59 vs. 73%; P = 0.003) when animals received 17.beta.-estradiol prior to PH. Findings in parenchymal cells from livers of growing rats were consonant with those observed in remnants after PH. The ERI of 5-day-old rats was only 9%. The value increased with maturity, reaching adult levels at 1 mo. (65%). Concomitantly, the labeling index, indicative of DNA synthesis, decreased from 30% in 5-day-old rats to 5% in 1-mo.-old animals. The temporal sequence of events, i.e., the appearance of nuclear ER, onset of DNA synthesis, and restoration of liver mass, permits formulation of a hypothesis which relates estrogen and its receptor to both the onset of hepatic regeneration after PH and liver growth in the neonate.