Cinnabar is Different from Mercuric Chloride in Mercury Absorption and Influence on the Brain Serotonin Level

Abstract

The toxicity of cinnabar, a naturally occurring mercury sulphide (HgS), has long been referred to soluble mercury chloride (HgCl 2 ). To investigate whether the speciation of mercury plays a role in its disposition and toxicity, we hereby investigated and compared cinnabar with soluble HgCl 2 and pure insoluble HgS in mice on mercury absorption, tissue distribution and in relation to the biological effects. The male C57BL/6J mice were treated by oral administration of various doses of cinnabar, with 0.01 g/kg of HgCl 2 for comparison, or the same dose of cinnabar or pure HgS (0.1 g/kg), once a day for 10 consecutive days. The total mercury contents in serum and tissue (brain, kidney, liver) were measured by atomic fluorescence spectrometer (AFS). The biological effects investigated involved monoamine neurotransmitters (serotonin, 5-HT) in brain as an indicator of therapeutic function, and serum alanine transaminase (ALT) as a marker of hepatic damage, blood urea nitrogen (BUN) and serum creatinine as markers for renal function. The mercury absorption of cinnabar or HgS was much less than that of HgCl 2 . The mercury levels in brains of the cinnabar group were only slightly changed and kept in a steady-state with the dose elevated. Cinnabar or HgS suppressed brain 5-HT levels. HgCl 2 could not cause any changes in brain 5-HT although the mercury level increased considerably. The results revealed that cinnabar or HgS is markedly different from HgCl 2 in mercury absorption, tissue distribution and influence on brain 5-HT levels, which suggests that the pharmacological and/or toxicological effects of cinnabar undertake other pathways from mercuric ions.

Comparison of mercury sulfides with mercury chloride and methylmercury on hepatic P450, phase-2 and transporter gene expression in mice

“…and MeHg in mice after 44 days of administration [6]. Thus, it is not surprising that in the current study (30 mg/kg, po for 7 days), no overt toxicological effects and gene expressions related to liver toxicity and drug processing genes were found, in agreement with the literature that the bioaccebility of HgS is quite different from HgCl2 [36,37], resulting in much less toxicity potential [26,38]. Compared to prior studies on the induction of Cyp1a, 3a, and 4a genes [26,38], no apparent effects of cinnabar on cytochrome P450 is evident under the present experimental conditions (lower dose and shorter time).…”

Mercury sulfides are much less nephrotoxic than mercury chloride and methylmercury in mice

“…We have previously shown that the kidney toxicity of HgS is much less than environmental mercurials in mice (300 mg/kg, po for 6 weeks) (Lu et al, 2011, and in rats (200 mg/kg, po for 60 days) (Shi et al, 2011). Thus, it is not surprising that in the current study (30 mg/kg, po for 7 days), no overt toxicological effects and gene expressions related to renal toxicity and transporters were found, in agreement with the literature about the bioaccebility of HgS (Koch et al, 2013;Wang et al, 2013;Tinggi et al, 2016) and our recent studies on cinnabar-containing traditional medicines on renal transporters (Zhu et al, 2014;Sui et al, 2015). However, it should be noted that the higher dose and longer-time of cinnabar administration, renal toxicity did occur (400-800 mg/kg, po for 90 days in rats) (Liang et al, 2009).…”

Chemical Compositions of Metals in Bhasmas and Tibetan Zuotai Are a Major Determinant of Their Therapeutic Effects and Toxicity

“…In mice treated with HgCl 2 (10 mg/kg) and 10-fold higher HgS (100 mg/kg) or cinnabar for 10 days, the Hg concentrations in the brain, serum, liver, and kidney of HgCl 2 -treated mice were 15-, 20, 65- and 87-fold higher than HgS groups, respectively. Most importantly, only HgS could significantly decrease brain serotonin levels, whereas HgCl 2 was ineffective [78].…”