Stress augmented ultraviolet-irradiation-induced pigmentation.

Area of Science:

• Endocrinology
• Dermatology
• Cell Biology

Background:

• Adrenocorticotropic hormone (ACTH) is known to stimulate melanogenesis in melanocytes.
• Stressful conditions, such as high population density and restraint, elevate ACTH levels in plasma and skin.
• Serum from stressed mice shows increased tyrosinase activity in human melanocytes, which is inhibited by corticostatin, an ACTH inhibitor.

Purpose of the Study:

• To investigate the association between circulating ACTH, induced by stress, and the regulation of ultraviolet (UV)-induced pigmentation.
• To determine if stress exacerbates UV-induced tanning and melanocyte proliferation.

Main Methods:

• Mice were divided into control, high population density, and restraint stress groups for 22 days.
• Animals were exposed to ultraviolet-B (UVB) irradiation thrice weekly.
• Changes in pigmentation, dihydroxyphenylalanine (DOPA)-positive melanocytes, and the effect of corticostatin pretreatment were assessed.

Main Results:

• Stressed mice exhibited delayed tanning and a significant increase in DOPA-positive melanocytes after UVB exposure.
• These stress-induced effects on pigmentation and melanocyte numbers were significantly inhibited by corticostatin pretreatment.
• Increased tyrosinase activity was observed in melanocytes exposed to serum from stressed mice.

Conclusions:

• Stress-induced ACTH may activate tyrosinase in melanocytes, augmenting UV-induced pigmentation.
• ACTH plays a role in the heightened sensitivity of the pigmentary response to UV irradiation under stressful conditions.
• These findings suggest a link between the endocrine stress response and skin pigmentation regulation.