Phototoxicity in Human Lens Epithelial Cells Promoted by St. John's Wort^¶

Abstract

St. John's Wort (SJW), an over‐the‐counter antidepressant, contains hypericin, which absorbs light in the UV and visible ranges and is phototoxic to skin. To determine if it also could be phototoxic to the eye, we exposed human lens epithelial cells to 0.1–10 μM hypericin and irradiated them with 4 J/cm2 UV‐A or 0.9 J/cm2 visible light. Neither hypericin exposure alone nor light exposure alone reduced cell viability. In contrast, cells exposed to hypericin in combination with UV‐A or visible light underwent necrosis and apoptosis. The ocular antioxidants lutein and N‐acetyl cysteine did not prevent damage. Thus, ingested SJW is potentially phototoxic to the eye and could contribute to early cataractogenesis. Precautions should be taken to protect the eye from intense sunlight while taking SJW.

Modifying excitation light dose of novel photosensitizer PVP-Hypericin for photodynamic diagnosis and therapy

“…The overdose of the excitation may result in an expansion of necrosis in cancer cells as well as sizeable morbidity in healthy surroundings since photosensitizers also accumulate in non-cancer cells [36][37][38].…”

Induction of keratinocyte apoptosis by photosensitizing chemicals plus UVA

“…Therefore, photosensitizing chemicals have only a phototoxic property or both phototoxic and photoallergic potentials. Apoptosis is usually considered to be one of the phototoxic outcome [22]. However, given that apoptotic cells bearing certain antigenic chemicals are easily Induction of keratinocyte apoptosis by photosensitizing chemicals plus UVA 109 captured and their antigenic determinants are presented by dendritic cells [14,15], apoptosis also seems to be closely related to the immunological response where T cells are primed.…”

Phototoxicity in Human Retinal Pigment Epithelial Cells Promoted by Hypericin, a Component of St. John’s Wort†

“…However, in our studies despite a reduction in mitochondrial activity, exposure of hRPE cells to visible light and/or hypericin did not result in a detectable increase in either mitochondrial or nuclear DNA lesions compared with untreated cells. Visible light exposure of RPE (11) and lens epithelial cells (12) pretreated with hypericin does induce apoptosis but probably through a lipid oxidation mechanism (43) rather than direct DNA damage.…”

“…If this transmitted light interacts with an accumulated photosensitizer, it can damage both the human lens and the retina (9). Hypericin is capable of crossing the blood–retinal barrier (5), and has been shown to induce apoptosis in retinal pigment epithelial (RPE) (11) and human lens epithelial cells (12). We have previously determined that hypericin is taken up by the intact lens (13) and RPE cells (14), binds to (15) and damages lens proteins (16), and distorts the transmission of light through the lens (17).…”