The ultrastructural effects of long-term use of henna on the albino rat skin

• Autores: Hani A. Al-Shobaili, Dalia R. El-Bassouny
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 29, Nº. 3, 2014, págs. 333-342
• Idioma: inglés
• Enlaces
  • Texto completo
• Resumen

  • Tattooing with henna is a routine practice in the Arab world. To the best of our knowledge, no previous studies have evaluated the adverse histological effects following henna tattooing on the ultrastructure of the skin. The objectives of this study were to diagnose the cytopathological alterations induced by commercial henna and to investigate the adverse role of henna when combined with sun ray on the skin. The skin of albino rats was tattooed with natural and black henna for three months, skin samples were examined by transmission electron microscope. In addition, the concentration of lead in henna samples was estimated by using atomic absorption spectrophotometry. The results expanded the understanding of the pathogenesis of henna-induced phytophotodermatitis. We hypothesized that henna-associated additives penetrated the epidermal barrier to gain access to the vascular dermis where the harmful ingredients became concentrated, leading to skin pathology through a dual mechanism. First, these ingredients became re-transported into the epidermis through vesicular trafficking leading to dermo-epidermal blistering and cytoplasmic vacuolization of the stratum basal cells. Following this, cytoplasmic vacuoles poured their content into the nuclei through continuities with the perinuclear cisterna, possibly leading to genetic mutation. The progression of keratinocytes into the next layers became associated with nuclear and cytoplasmic signs of apoptosis with subsequent phagocytosis in other epidermal cells, most probably keratinocytes. The second mechanism of injury was mediated through accumulation of inflammatory cells around capillaries in the dermis with the release of angiogenic and mitogenic mediators resulting in vasculopathy.