It is likely to exert this effect by binding to specific nuclear receptors (members of the retinoic acid receptor or retinoid X receptor nuclear transcription family) which are found in every cell (including osteoblasts and osteoclasts).This change in bone turnover is likely to be the reason for numerous effects seen in hypervitaminosis A, such as hypercalcemia and numerous bone changes such as bone loss that potentially leads to osteoporosis, spontaneous bone fractures, altered skeletal development in children, skeletal pain, radiographic changes, and bone lesions. Altered fat-soluble vitamin metabolism
Preformed vitamin A is fat-soluble and high levels have been reported to affect metabolism of the other fat-soluble vitamins D, E, and K.
The toxic effects of preformed vitamin A might be related to altered vitamin D metabolism, concurrent ingestion of substantial amounts of vitamin D, or binding of vitamin A to receptor heterodimers. Antagonistic and synergistic interactions between these two vitamins have been reported, as they relate to skeletal health. Stimulation of bone resorption by vitamin A has been reported to be independent of its effects on vitamin D.

Mitochondrial toxicity
Preformed vitamin A and retinoids exerts several toxic effects regarding redox environment and mitochondrial function. Diagnosis
Retinol concentrations are nonsensitive indicators
Assessing vitamin A status in persons with subtoxicity or toxicity is complicated because serum retinol concentrations are not sensitive indicators in this range of liver vitamin A reserves. The range of serum retinol concentrations under normal conditions is 1–3 μmol/L and, because of homeostatic regulation, that range varies little with widely disparate vitamin A intakes.
Overconsumption of beta-carotene can only cause carotenosis, a harmless and reversible cosmetic condition in which the skin turns orange. Preformed vitamin A absorption and storage in the liver occur very efficiently until a pathologic condition develops. When ingested, 70–90% of preformed vitamin A is absorbed and used. Sources of toxicity
Diet – Liver is high in vitamin A. The liver of certain animals, including the polar bear, bearded seal, fish, walrus, and moose, are particularly toxic (see Liver (food) § Poisoning). It has been estimated that consumption of 500 grams of polar bear liver would result in a toxic dose for a human. Supplements – Dietary supplements can be toxic when taken above recommended dosages. Types of toxicity
Acute toxicity occurs over a period of hours or a few days, and is less of a problem than chronic toxicity. Chronic toxicity results from daily intakes greater than 25,000 IU for 6 years or longer and more than 100,000 IU for 6 months or longer. Mechanism
Absorption and storage in the liver of retinol occur very efficiently until a pathologic condition develops. Delivery to tissues
Absorption
When ingested, 70–90% of preformed vitamin A is absorbed and used.According to a 2003 review, water-miscible, emulsified, and solid forms of vitamin A supplements are more toxic than oil-based supplement and liver sources. Storage
80–90% of the total body reserves of preformed vitamin A are in the liver (with 80–90% of this amount being stored in hepatic stellate cells and the remaining 10–20% being stored in hepatocytes).