Kim, Y, JC Ryu, H Choi and K Lee. 2011. Effect of 2,2,'4,4'-tetrahydroxybenzophenone (BP2) on steroidogenesis in testicular Leydig cells. Toxicology http://dx.doi.org/10.1016/j.tox.2011.06.013

A UV-blocking chemical added to stabilize personal care products works as an endocrine disruptor and reduces the production of male reproductive hormones.

Researchers show an ultraviolet (UV) radiation blocker - designated BP2 - found in a variety of cosmetics and personal care products decreases testosterone hormone production in both cultured human testes cells and in male mice.

This is the first study to report that BP2 exposure can impact reproductive processes in mammals, including human cells. The new findings - when combined with results from prior studies - suggest more research is needed to understand if BP2 poses endocrine-related health risks when used to stabilize personal care products.

Benzophenone (BP) chemicals absorb and thus filter out ultraviolet light. The one known as BP2 is added to cosmetics and personal care products to prevent sunlight from breaking down the products. Perfumes, lipstick, hair and skin care products and plastics for packaging can contain BP2. People can be exposed as BP2 has been detected in human urine.

Prior research suggests BP2 can interfere with hormones important to reproduction, most notably thyroid hormones. The chemical can inactivate a key enzyme involved in thyroid hormone production, according to human cell line studies. Of its many functions, thyroid hormone promotes testosterone production in the male testes and increases levels circulating in the blood of lab animals and humans. Thus, less thyroid hormone levels could reduce testosterone production.

Even so, little research deals with how BP2 may affect reproductive hormones in people and mammals. Therefore, researchers investigated if BP2 could disrupt thyroid hormone signals that, in turn, would alter the testes' ability to produce testosterone.

A two-tiered approach was used. The researchers exposed human testes cells to BP2 in the lab. They also injected 5-week-old male mice with 50 milligrams/kilogram/body weight of BP2 and sampled their testes and blood. Both the lab cells and the mice testes were analyzed for genetic and protein markers. Testosterone and progesterone hormones were measured in lab cells and the mouse testes and blood.

The results showed that BP2 does impact testicular hormone production, leading to reduced levels of the important male reproductive hormone testosterone. However, BP2 acted in an opposite manner on the levels of steroid producing enzymes that are controlled by thyroid hormone signaling. It dampened the genes that thyroid hormone stimulates and stimulated genes that thyroid hormone dampens. This effect of BP2 was observed even in the absence of thyroid hormone, so more was occurring than just direct antagonism of thyroid hormone signaling by BP2.

In other words, BP2 decreased male testosterone production in ways not always directly related to impeding normal thyroid hormone signals. The results suggest a mixed bag. BP2 has anti-thyroid activity - as prior research shows - but also may interfere with other types of hormone signals, such as acting as an estrogen.

Further research will be needed to tease apart the exact role BP2 plays as an endocrine disruptor and how its effects lead to reduced testosterone levels.