Are Zhusha or Shengtieluo effective or recommended to Calm Shen?

[Guest guest]

Hi Shanna

 

> Zhusha is considered toxic. It is not available [for medicinal use]

> although I live in an old cinnabar mining district and it is all

> over the ground here in its raw state. My biology professors

> insisted it was not toxic in its raw form because the temperature

> has to be raised considerably to isolate the mercury which is the

> toxic component.

 

Some people believe that insoluble mercury salts are non-toxic.

IMO, that belief is incorrect. Sure, the soluble salts are more toxic

than the insoluble ones, but the latter are also absorbed via the

lungs, gut and skin, and accumulate in tisues; they ARE TOXIC at

high doses. See references, below. Your biology professors may

change their opinions when they read these.

 

> In the form of cinnabar, used unheated (it is usually added as a

> powder at the end of decoction) I wonder if it is less dangerous

> than the FDA would have us assume.

 

Yes, heated cinnabar can release mercury vapour, which is highly

toxic if inhaled. However, cinnabar absorption still occurs via the

oral route, and via skin, if used topically.

 

Also, Zhusha may not be as effective as other medicaments to

Calm Shen. For example, Suanzaoren Anshen capsules were

more effective than Zhusha Anshen pills in one Chinese trial (Ma &

Li 1989, see references, below).

 

> At least the mercury doesn't end up in the water supply here--it is

> bound up in compounds within the cinnabar.

 

Again, IMO, this is questionable. Insoluble and complexed mercury

salts are less mobile in soil than soluble forms, but microbial

action (in soil) can convert even complexed salts into highly toxic

methylmercury. Also, rain-fall and dust-blow can move

contaminated soil into surface water. FIsh living there, especially

bottom-feeders like catfish and bream, accumulate mercury in their

tissues,

 

> I am unable to find a distributor for Shengtieluo (iron filings).

> They hadn't even heard of it at Mayway. I was wondering if it would

> be ok to use an industrial source for iron filings and if further

> processing is necessary for it to be used in decoction. There is no

> toxicity mentioned in Bensky associated with Shengtieluo.

 

There may be two reasons why it is hard to find suppliers.

 

(a) Shengtieluo (Frusta Ferri) is classed as a medicinal to Calm

Shen & Build HT. However, a Google search for hits for (indicating

usage and sales of) Shengtieluo suggests that it is used much

more rarely than other medicaments in that class. For example,

Google has only 11 hits for Shengtieluo OR Sheng-tie-luo, whereas

it has 3140 hits for Longgu OR Long-Gu

 

(b) Crude Shengtiluo may contain heavy metals (such as As, Hg,

Cd, etc) as contaminants. It may be that Drug Regulation agencies

allow only purified Shengtieluo (refined to remove contaminants) for

oral use in humans.

 

> I am using Longgu as a substitute but was wondering why I can't

> find anyone that knows about Shengtieluo. It would be desirable

> over Longgu for this pattern as it has no astringing properties and

> the pattern, Phlegm Fire Harrasing HT, is an excess pattern. I'd

> appreciate any further comment on Shengtieluo or sources for it.

> Thanks, Shanna

 

Perhaps other Listers would comment on that?

 

Best regards,

Phil

 

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

 

Chuu-Jiunn-Jye, Hsu-Chuan-Jen, Lin-Shiau-Shoei-Yn. | Abnormal

auditory brainstem responses for mice treated with mercurial

compounds: Involvement of excessive nitric oxide. | Toxicology,

April 12th, 2001, vol. 162, no. 1, p. 11-22, | Lin-Shiau-Shoei-Yn,

Institutes of Toxicology, College of Medicine, National Taiwan

University, Jen-Ai Road, No. 1, Section 1, Taipei, 10043, Taiwan.

Email: syl. | In this paper, we attempted to

construct an animal (mouse) model for monitoring the oto-

neurotoxicity of mercuric sulphide, comparing its toxicity with the

well-known (organic) mercury compound methyl- mercury. Mice

were treated with either mercuric sulphide (HgS, 0.1 and 1.0 g/kg

per day) or methyl-mercury (MeHg, 0.2, 2.0 and 10 mg/kg per day)

by gastric gavage for 7 consecutive days. Analysis of auditory

brainstem response (ABR) indicated that significant elevation of the

physiological hearing threshold as well as significant prolongation

of interwave latency I-V was observed for MeHg - (2.0 and 0.2

mg/kg per day) or HgS - (1.0 g/kg per day, but not 0.1 g/kg per

day) treated mice. Further, both MeHg- and HgS-treated animals

demonstrated a significant prolongation of interwave latency I-V

that increased with an increasing mean blood-Hg level. The oto-

neurotoxicity of MeHg (2.0 mg/kg per day) persisted to at least 11

weeks subsequent to the cessation of its administration. The toxic

effect of HgS, however, disappeared completely 5 weeks

subsequent to the cessation of its administration. These results

suggest a correlation between the Hg-elicited hearing dysfunction

and the availability of mercury in brain tissue. Both inhibition of

Na+/K+-ATPase activity and overproduction of nitric oxide in the

brainstem are consistent with an analysis of the physiological

hearing threshold and latencies of ABR waveform at all time points

throughout the experimental process. Thus, it is proposed that high-

dose HgS or MeHg intoxication is associated with a decrease in

functional Na+/K+-ATPase activity in the brainstem of affected

animals, this presumably arising via excessive nitric oxide

production, and suggesting that brainstem damage may play a role

in mercury-induced hearing loss.

 

Chuu-Jiunn-Jye, Liu-Shing-Hwa, Lin-Shiau-Shoei-Yn. | Effects of

methyl mercury, mercuric sulphide and cinnabar on active

avoidance responses, Na+/K+-ATPase activities and tissue

mercury contents in rats. | Proceedings of the National Science

Council Republic of China Part B Life Sciences, April, 2001, vol.

25, no. 2, p. 128-136, | Lin-Shiau-Shoei-Yn, College of Medicine,

Institutes of Toxicology, National Taiwan University, Taipei, Taiwan.

| This study compared the neurobehavioral toxicities of three

mercurial compounds: methyl mercury (MeHg) which is soluble

and organic, and mercuric sulphide (HgS) and cinnabar (naturally

occurring HgS), which are insoluble and inorganic. Cinnabar, a

Chinese mineral medicine, is still used as a sedative in some

Asian countries, but there is relatively little toxicological information

about it. These mercurial compounds were administered

intraperitoneally (MeHg, 2 mg/kg) or orally (HgS and cinnabar, 1.0

g/kg) to male rats once every day for 13 consecutive days with

assays conducted during or after discontinuous administration for 1

h, 2, 8 and 33 weeks. Neurotoxicity was assessed based on the

active avoidance response and locomotor activity. The results

obtained showed that MeHg and cinnabar prominently and

irreversibly caused a decrease in body weight, prolongation of

latency for escape from electric shock, a decrease in the

percentage for the conditioned avoidance response (CAR) to

electric shock, impairment of spontaneous locomotion and

inhibition of Na+/K+-ATPase activity of the cerebral cortex. In

contrast, HgS reversibly inhibited spontaneous locomotion and

Na+/K+-ATPase activity. It was noted that HgS significantly

decreased the latency of escape from electric shock during the

administration period, which lasted for 33 weeks after

discontinuous administration. In fact that pretreatment with

arecoline (a cholinergic receptor agonist) but not fipexide (a

dopaminergic receptor agonist) could significantly shorten the

prolonged latency for escape caused by MeHg and cinnabar,

suggested that the deficit in the active avoidance response was

perhaps, at least in part, mediated by the dysfunction of the

cholinergic rather than the dopaminergic system. Determination of

the Hg levels of the whole blood and cerebral cortex revealed that

the tissue mercury content was highly correlated with the degree of

neurobehavioral toxicity of these Hg compounds. These findings

suggest that insoluble HgS and cinnabar can be absorbed from the

G-I tract and distributed to the brain. The possibility that

contamination due to other minerals in the cinnabar is responsible

for the greater neurotoxic effects compared to HgS is under

investigation.

 

Chuu-J-J, Young-Y-H, Liu-S-H, Lin-Shiau-S-Y. | Neurotoxicity of

mercury sulphide in the vestibular ocular reflex system of guinea

pigs. | Naunyn-Schmiedeberg's archives of pharmacology {Naunyn-

Schmiedebergs-Arch-Pharmacol} 2001 Sep, VOL: 364 (3), P: 249-

58, ISSN: 0028-1298. | Institute of Toxicology, College of Medicine,

National Taiwan University, No. 1, Section 1, Jen-Ai Road, Taipei,

Taiwan, ROC. | Zhusha, a traditional Chinese mineral medicine,

cinnabar, naturally occurring mercuric sulphide (HgS), is still

occasionally prescribed, but the neurotoxic effects of HgS have not

been elucidated. In this paper, an animal model of the purified HgS

intoxication was established in guinea pigs in order to study

neurotoxicity and pathophysiology of the vestibular ocular reflex

system (VOR). Guinea pigs were dosed with HgS by gastric

gavage (0.01, 0.1 and 1.0 g/kg per day) for 7 consecutive days. By

means of caloric testing coupled with the electronystagmographic

(ENG) recording in guinea pigs, we have found that HgS at a dose

of 0.1 g/kg induced reversible caloric hypofunction pattern and at a

higher dose of 1.0 g/kg induced irreversible hypofunction of caloric

test. Monitoring the mercury contents of various tissues (blood,

kidney, liver and cerebellum) by continuous flow and cold vapor

atomic absorption spectrometry (AAS) revealed that a certain

amount of HgS could be absorbed from the gastrointestinal tract

and was detectable in these tissues. In addition to the induced

dysfunction of VOR system, HgS also caused disturbance of motor

performance in guinea pigs. In enzyme assay, Na+/K+-ATPase

activity of cerebellum was also significantly inhibited by HgS.

Morphological studies showed partial cell loss only in the

cerebellar Purkinje cell layer, but not in the granule cell layer, nor

in the vestibular labyrinth. All of these findings suggest that

cerebellar Purkinje cells are the sensitive target site responsible for

HgS-inducing dysfunctions of both VOR system and the motor

performance in guinea pigs. Thus, it is concluded that caloric test

coupled with ENG recording in VOR system is certainly a sensitive

biomarker for monitoring the neurotoxicity of HgS.

 

Ghazi-A-M, Reinhard-K-J, Holmes-M-A, Durrance-E. | Further

evidence of lead contamination of Omaha skeletons. | American

journal of physical anthropology {Am-J-Phys-Anthropol} 1994 Dec,

VOL: 95 (4), P: 427-34, ISSN: 0002-9483. | Dept of Geology,

University of Nebraska-Lincoln 68588-0340. | A previous analysis of

Omaha skeletons dating between A.D. 1780 and 1820 revealed the

presence of lead in all skeletons with high concentrations in

children and adult males (Reinhard and Ghazi (1992) Am. J. Phys.

Anthropol. 89:183-195). Two likely explanations for the high lead

levels were presented: 1) metabolic absorption of lead and 2)

diagenetic uptake of lead by the bones from postmortem

application of pigments to the corpse. Two types of lead were

available to the Omaha tribe: 1) Mississippi Valley type, and 2) non-

Mississippi Valley type. It has been suggested that red-lead

pigment mixed with mercury sulphide (cinnabar) applied to the

corpse may have been one of the sources of lead found in bones.

Further isotopic analyses of samples of pigment and metallic lead

artifacts associated with the skeletons revealed that non-

Mississippi Valley type lead is present in the pigment while

Mississippi Valley type lead comes from metallic artifacts. Both

lead and mercury were found in the pigment samples, verifying that

a lead-based pigment mixed with cinnabar-based pigment was

used as a cosmetic by the Omaha. Isotopic analysis of lead in

skeletons indicates that the pigment contributed most to lead

content of bone. This new evidence clarifies the previous study and

suggests specific mechanisms by which lead became incorporated

into bone.

 

Ho-Bryan-S-J, Lin-Ja-Liang, Huang-Chung-Chi, Tsai-Ying-Huang,

Lin-Meng-Chih Email: mengchih. | Mercury

vapor inhalation from Chinese red (Cinnabar). | Journal of

Toxicology Clinical Toxicology, January 2003, vol. 41, no. 1, p. 75-

78, | Lin-Meng-Chih, 5 Fu-Hsin St. Kwei-Hsan, Taoyuan, 333,

Taiwan. | Introduction: Acute inhalation of mercury fumes or vapors

is a rare but frequently fatal cause of acute lung injury. This report

describes a rare cause of mercury inhalation from Chinese red.

Case Report: An 87-year-old male inhaled the vapors from heating

Chinese red (Cinnabar, mercury sulphide) intended to treat his foot

ulceration. He subsequently developed acute lung injury

(progressive dyspnea and acute respiratory failure) that was treated

with mechanical ventilation. DMPS (2,3-Dimercapto-1-

propanesulphonic acid) and penicillamine were used as chelating

agents, and methylprednisolone pulse therapy was used to treat

his pulmonary disease. Despite being extubated once, the patient

eventually died from profound hypoxemia. Conclusion: A rare case

of mercury intoxication was due to inappropriate use of an

alternative medicine, Chinese red. This case serves as a reminder

of the toxicity of the noxious gas from this substance and the

importance of being familiar with alternative medicines.

 

Kang-Yum-E, Oransky-S-H. | Chinese patent medicine as a

potential source of mercury poisoning. | Veterinary and human

toxicology {Vet-Hum-Toxicol} 1992 Jun, VOL: 34 (3), P: 235-8,

ISSN: 0145-6296. | Hudson Valley Poison Control Center, Nyack,

NY 10960. | This research is an effort to create awareness of the

potential hazards of some Chinese patent medicines which contain

mercurial ingredients. This should be of consideration when

screening symptomatic patients who are of Asian ethnic

background or other users of these medicines. This research

discusses reported cases of mercury poisoning related to the use

of Chinese patent medicines and the potential toxicity of cinnabar

(red mercuric sulphide) and calomel (mercurous chloride), 2

mercurials commonly used in these medicines. A list of mercurial-

containing Chinese patent medicines available on the open market

in North America has been compiled, together with their traditional

uses and mercurial contents and is presented as a quick reference

for Specialists in Poison Information. This class of medicine may

not pose a problem when used appropriately; however, its misuse,

abuse, overdosage and improper storage can lead to serious

mercury poisoning.

 

Magos-L. | Mercury and mercurials. | British Medical Bulletin; vol

31; no 3; pp 241-245; ISSN: 0007-1420. Publication year 1975. |

Medical Research Council, Toxicology Unit, Carshalton, Surrey,

UK. | Although 70M tons of mercury are present in the sea, and

30K tons are precipitated on the land by rain each year, the real

problem of mercury pollution arises from the localized increase in

its production by industrial and other processes. 20K tons were

produced each year from 1965-75, concentrated in a relatively few

locations. On land, mercury compounds are either detoxified by

conversion to mercuric sulphide, or volatilized as mercuric oxide.

Mercury is retained in plant roots, so that levels in plant products,

and products of animals which feed on them, remain safe. In water,

some mercury is converted to mercuric sulphide, but much is

methylated by bacteria, and toxic methylmercury is accumulated

in fish muscle even against a steep concentration gradient. Levels

of 0.5-14 ppm mercury have been found in various species of fish.

Air can be contaminated by evaporation from mercury or solutions

of its ionized salts. Mercury vapour is absorbed through the alveolar

membrane and is oxidized in blood and tissues before reacting with

sulphydryl groups on proteins. Its selective toxicity probably

depends on the time it takes to be fully oxidized, and its

distribution in that time. The toxic effects can usually be reversed

by treatment. Mercuric and mercurous chloride are the most

common toxic salts of mercury. The former is concentrated in the

kidneys, but the condition can be treated if the dose was not too

high. Organomercurials are found in fungicides and diuretics, and

are theoretically less toxic than inorganic mercury salts, but are

rapidly transformed to inorganic salts in the liver. However, they are

more slowly absorbed than inorganic mercury, so that the diuretics

do not cause concentration of mercury in the kidney. The author

concludes that the main danger of mercury lies in its conversion by

bacteria to methylmercury, which is concentrated by fish muscle,

has a long half-life (70 days), crosses the placenta, and causes

irreversible brain damage. Cases of toxicity usually involve acute

rather than chronic exposure. Control of mercury pollution in the

future should be sufficient to prevent mercury toxicity from

becoming a severe or world-wide problem.

 

Ma-Y-D, Li-R-H. | (Observation on the efficacy and experimental

study of compound suanzaoren ansen capsules in insomnia). |

Zhong xi yi jie he za zhi {Zhong-Xi-Yi-Jie-He-Za-Zhi} 1989 Feb,

VOL: 9 (2), P: 85-7, 68-9, ISSN: 0254-9034. | | 374 patients

suffering from insomnia were divided into three groups by random:

202 cases in group I were treated with compound Suanzaoren

Ansen capsules (SAC); 85 cases in group II were treated with

Zhusha Ansen pills (ZAP) as control; 87 cases in group III were

treated with Methaqualone (Hyminal) also as control. The

therapeutic results were as follows: Groups I, II and III showed

significant effective rates of 49.50%, 18.82% and 32.18%

respectively; moderate effective rates of 34.65%, 48.24% and

49.43% respectively; and total rates of effectiveness of 84.15,

67.06% and 81.61% respectively. The authors found significant

statistical difference between group I and II (P less than 0.005) and

of no statistical difference between group I and III (P greater than

0.05). The results showed that the effects of compound SAC were

better than ZAP, and similar to that of methaqualone. EEG

analysis carried out while sleeping confirmed the effects mentioned

above. Low toxicity (LD50 10.7 g/kg) of compound SAC was found

through animal experimentations. No towards reactions were

revealed in clinical trials except nausea in 3 cases. Heart rate and

blood pressure changed lightly in a few cases.

 

Sin-Y-M, Teh-W-F. | Effect of long-term uptake of mercuric sulphide

on thyroid hormones and glutathione in mice. | Bulletin of

Environmental Contamination and Toxicology, 1992, vol. 49, no. 6,

p. 847-854, | Sin-Y-M, Dep. Zool., Natl. Univ. Singapore, Lower

Kent Ridge Road, Singapore 0511, Singapore. |

 

Tan-T-M, Sin-Y-M, Wong-K-P. | Mercury-induced UDP-

glucuronyltransferase (UDPGT) activity in mouse kidney. |

Toxicology {Toxicology} 1990 Oct, VOL: 64 (1), P: 81-7, ISSN:

0300-483X. | Dept of Biochemistry, National University of

Singapore. | Administration of mercuric chloride to young adult

mice produced a significant increase in the activity of renal UDP-

glucuronyltransferase (UDPGT) measured with harmol as the

acceptor substrate. This was observed 10 days after a daily oral

dose of HgCl2 (6 micrograms Hg2+/g body wt.). The increase in

UDPGT activity was correlated with an accumulation of mercury in

the renal tissues and was accompanied by an increase in the

apparent Vmax of the glucuronidation reaction without a change in

the apparent Km values for harmol or UDPGA. Parallel studies with

mercuric sulphide however showed negligible retention of mercury

in both the liver or kidney nor was there any change in UDPGT

activity compared to control values. The difference in solubilities of

the two mercuric salts may be responsible for this observation. The

possible mode of activation of UDPGT by mercury treatment is

discussed.

 

USA, Centers for Disease Control. | Elemental mercury vapor

poisoning: North Carolina, 1988. | Morbidity and Mortality Weekly

Report; vol 38; no 45; pp 770-772, 777; ISSN: 0149-2195.

Publication year 1989. | | This short case report describes the

mercury vapour poisoning of a 3-year-old boy whose family had

moved house 3 months earlier. The patient had hypersalivation,

myalgia and tremor in the hands, myalgia and weakness in both

lower extremities, profuse perspiration, irritability, insomnia,

anorexia and a 360 micro g/l urinary concentration of mercury. The

mother had 230 micro g/l and the father 145 micro g/l urinary

mercury. The child was treated with penicillamine. Extensive

investigation of the house revealed 20-60 micro g/m3 Hg

concentrations in 5 rooms and 2 bathrooms. In the bedroom of the

patient the concentration was 55 micro g/m3 (range 30-140).

Mercury concentrations in a dust sample in the vacuum cleaner

bag and carpets were 4400 p.p.m. and 0.8-638 p.p.m. respectively.

The origin of the mercury was traced back to the previous owner

who was a collector of liquid mercury. His children had also

elevated urinary mercury concentrations (98 and 49 micro g/l) but

no signs of mercury intoxication. Corrective measures included the

temporary removal of the family from the house, removal of the

carpets, and decontamination of surfaces by conversion of liquid

mercury into mercury sulphide. Laszlo Magos.

 

Wild-L-G, Ortega-H-G, Lopez-M, Salvaggio-J-E. | Immune system

alteration in the rat after indirect exposure to methyl mercury

chloride or methyl mercury sulphide. | Environmental research

{Environ-Res} 1997, VOL: 74 (1), P: 34-42, ISSN: 0013-9351. |

Dept of Medicine, Tulane University Medical School, New Orleans,

Louisiana 70112, USA. | Methyl mercury is a well-recognized

health hazard. It is an environmental contaminant that accumulates

in the food chain. The primary source of mercury exposure for

humans is through the consumption of contaminated fish. We

studied the effects of indirect methyl mercury exposure on the

immune system of Sprague-Dawley rats. The effects of different

forms of methyl mercury on immune system development were

studied in Sprague-Dawley rats at 6 and 12 weeks of age. Rats

were indirectly exposed to mercury during gestation and during

nursing by exposing pregnant rats to either 5 or 500 micrograms

/liter of methyl mercury chloride (CH3HgCl) or 5 micrograms/liter of

methyl mercury sulphide ((CH3Hg)2S) in their drinking water. Total

body, splenic, and thymic weights were measured, and NK cell

cytolytic activity and lymphoproliferative response to T and B cell

mitogens were evaluated in the offspring. At 6 weeks of age, total

body and splenic weights were significantly increased in both high-

and low-dose methyl mercury chloride-exposed groups. Rats

exposed to methyl mercury sulphide had a significant increase in

thymic weight at 6 weeks of age. At 12 weeks, the total body and

organ weights were not different from controls. The lymphocyte

proliferative response of splenocytes to PWM was enhanced at 6

weeks in both CH3HgCl exposed groups and not affected in the

(CH3Hg)2S exposed group. NK cell activity was not affected in

either group at 6 weeks of age. At age 12 weeks, NK cell activity

was statistically significantly decreased by 56.6% in both CH3HgCl-

exposed groups and not affected in the (CH3Hg)2S-exposed rats.

The lymphocyte proliferative response of splenocytes to the B cell

mitogen pokeweed remained increased in the CH3HgCl groups.

Indirect exposure of rats (during gestation and nursing) to different

forms of methyl mercury reveals that chloride forms have prolonged

predominantly enhancing effects on lymphoproliferative response of

splenocytes, followed by significant depression of NK cell activity.

 

Yeoh-T-S, Lee-H-S, Lee-A-S. | Gastrointestinal absorption of

mercury following oral administration of cinnabar in a traditional

Chinese medicine. | Asia Pacific Journal of Pharmacology; vol 4;

no 2; pp 69-73; ISSN: 0217-9687. Publication year 1989. | Dept

Pharmacol, Nat Univ Singapore, Kent Ridge, Singapore 0511. |

Fourteen of 99 preparations of traditional Chinese medicine

purchased in Singapore and Malaysia had >0.5 micro g/g, 8 had

>10 micro g/g and 7 >1 mg/g of mercury, most likely in the form of

cinnabar (mercuric sulphide). Cinnabar according to Chinese

traditional medicine has detoxifying and tranquilizing properties.

These authors tested the effect of the ingestion of 1 preparation on

the urinary excretion of mercury in mice and in 2 volunteers. The

preparation, recommended for neurasthenia, dizziness, insomnia,

general debility, lumbago, and poor memory, contained 2.57 mg

mercury/pill. It was mixed with the food of mice to give a

concentration of 1.5 mg mercury/g. This food given to mice for 6

days resulted in a total intake of 18 mg mercury/mouse and

increased the urinary excretion of mercury in the treatment period

by about 1.8 ng/hour. On the seventh day the animals were killed

for mercury analysis in kidneys and liver. The hepatic mercury

concentration increased from 0.031 to 0.27 micro g/g and the renal

mercury concentration from 0.071 to 1.5 micro g/g. Two of the

investigators took the recommended dose of 5 pills 3 times a day

for a single day. The 15 pills contained 38.5 mg mercury. On

average their daily urinary excretion of mercury increased by 10.5

ug in the following 3 days. The total mercury excretion in the first

day after ingestion was 20.3 ug in one person and 16.2 ug in the

other. (Although this urinary excretion accounts for only a small

part of the ingested dose, it is not insignificant and indicates that

not all the ingested cinnabar is passed with stool.)

 

Young-Yi-Ho, Chuu-Jiunn-Jye, Liu-Shing-Hwa, Lin-Shiau-Shoei-Yn.

| Neurotoxic mechanism of cinnabar and mercuric sulphide on the

vestibulo-ocular reflex system of guinea pigs. | Toxicological

sciences {Toxicol-Sci} 2002 Jun, VOL: 67 (2), P: 256-63, ISSN:

1096-6080. | Dept of Otolaryngology, National Taiwan University

Hospital, No. 1 Section 1, Jen-Ai Road, Taipei, Taiwan. | Cinnabar,

a naturally occurring mercuric sulphide (HgS), has been combined

with Chinese herbal medicine as a sedative for more than 2000

years. To date, its neurotoxic effect on the vestibulo-ocular reflex

(VOR) system has not been reported. By means of a caloric test

coupled with electronystagmographic recordings, the effect of

commercial HgS and cinnabar on the VOR system of guinea pigs

was studied. HgS or cinnabar was administered orally (1.0 g/kg) to

Hartley-strain guinea pigs once daily for 7 consecutive days. A

battery of electrophysiological, biochemical, and histopathological

examinations were performed. The results showed that HgS

induced a 60% caloric response abnormality (40% caloric

hyperfunction and 20% hypofunction), whereas the abnormal

responses appeared to be more severe (six out of six) in the

cinnabar group. The Hg contents of whole blood and cerebellum

were increased and correlated to their neurotoxic effects on the

VOR system, indicating that both insoluble HgS and cinnabar

could be absorbed from the gastrointestinal tract and distributed to

the cerebellum. Although the vestibular labyrinth revealed no

remarkable change under light microscopy, loss of Purkinje cells in

the cerebellum was detected, and the enzymatic Na(+)/K(+)-

ATPase activity of cerebellum (a higher inhibitory center of the

VOR system) was significantly inhibited by HgS and cinnabar.

Moreover, cerebellar nitric oxide (NO) production was increased

significantly. Hence, we tentatively conclude that the increased Hg

contents in the cerebellum following oral administration of HgS and

cinnabar were responsible, at least in part, for the detrimental

neurotoxic effect on the VOR system. Potentially, decreasing

Na(+)/K(+)-ATPase activity and increasing NO production within

the cerebellar regulatory center are postulated to mediate this VOR

dysfunction caused by the mercurial compounds and cinnabar.

 

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

 

 

Best regards,

 

Email: <

 

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[Guest guest]

I'll quickly tell my zhusha story which is really Al Stone's as well. A

Taiwanese friend said

her mother had brought an amazing healer in from Taiwan and was seeing lots of

patients at my friends house. However she need Zhusha to treat some people and

did I

have any access to any? I asked Al who said he would give her some but he wanted

to

see what and how she was going to use it.

So that night we drove out to the San Gabriel Valley (a lot of Chinese there)

outside of

Los Angeles. The woman was doing a sort of a cross between Catholic exorcism and

Qi

Gong on a few patients. She took the Zhusha and mixed it with water in the

kitchen. We

were in anticipation. How much would she have them take? Would she mix it with

other

herbs? We went into the room with the patients and she proceeded to use the

Zhusha as

an ink and with a brush, drew Chinese charactors of buddhist phrases on the

patients

backs! I guess there is all types of healing modalities out there! As I

remember she

quickly washed the charactors away, hopefully no toxins were passed through the

skin.

doug

 

 

, " " <@e...>

wrote:

> Hi Shanna

>

> > Zhusha is considered toxic. It is not available [for medicinal use]

> > although I live in an old cinnabar mining district and it is all

> > over the ground here in its raw state. My biology professors

> > insisted it was not toxic in its raw form because the temperature

> > has to be raised considerably to isolate the mercury which is the

> > toxic component.

>

> Some people believe that insoluble mercury salts are non-toxic.

> IMO, that belief is incorrect. Sure, the soluble salts are more toxic

> than the insoluble ones, but the latter are also absorbed via the

> lungs, gut and skin, and accumulate in tisues; they ARE TOXIC at

> high doses. See references, below. Your biology professors may

> change their opinions when they read these.

>

> > In the form of cinnabar, used unheated (it is usually added as a

> > powder at the end of decoction) I wonder if it is less dangerous

> > than the FDA would have us assume.

>

> Yes, heated cinnabar can release mercury vapour, which is highly

> toxic if inhaled. However, cinnabar absorption still occurs via the

> oral route, and via skin, if used topically.

>