Abstract
The aim of this study was to explore the role of apoptosis in cinnabar-induced renal injury in rats. To test this role, rats were dosed orally with cinnabar (1 g/kg/day) for 8 weeks or 12 weeks, and the control rats were treated with 5% carboxymethylcellulose solution. Levels of urinary mercury (UHg), renal mercury (RHg), serum creatinine (SCr), and urine kidney injury molecule 1 (KIM-1) were assessed, and renal pathology was analyzed. Apoptotic cells were identified and the apoptotic index was calculated. A rat antibody array was used to analyze expression of cytokines associated with apoptosis. Results from these analyses showed that UHg, RHg, and urine KIM-1, but not SCr, levels were significantly increased in cinnabar-treated rats. Renal pathological changes in cinnabar-treated rats included vacuolization of tubular cells, formation of protein casts, infiltration of inflammatory cells, and increase in the number of apoptotic tubular cells. In comparison to the control group, expression of FasL, Fas, TNF-α, TRAIL, activin A, and adiponectin was upregulated in the cinnabar-treated group. Collectively, our results suggest that prolonged use of cinnabar results in kidney damage due to accumulation of mercury and that the underlying mechanism involves apoptosis of tubular cells via a death receptor-mediated pathway.
Highlights
Cinnabar is a naturally occurring mercuric sulfide (HgS ≥ 96%) [1]
Our results suggest that cinnabar-induced renal injury is associated with increased apoptosis of tubular cells and that death receptors play a primary role in activation of this apoptotic pathway
Weight gain, or activity of the cinnabar-treated rats were observed in comparison with the controls
Summary
Cinnabar is a naturally occurring mercuric sulfide (HgS ≥ 96%) [1]. Cinnabar powder has been used as an important ingredient in traditional Chinese medicines and in Indian Ayurvedic medicines [2] for more than 2000 years. Cinnabar is generally thought to be slight toxic because HgS is almost insoluble in water, adverse reactions to cinnabar or cases of intoxication have occasionally been reported in the clinical literature [7,8,9,10]. These toxicities primarily result from inappropriate usage, such as excessive and long-term dosage [10]. Excessive or long-term use of cinnabar or cinnabar-containing preparations can result in renal dysfunction due to accumulation of mercury [10]. Several studies have reported the renal toxicity of cinnabar, the underlying mechanism associated with this toxicity remains unclear
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