revised final - Agency for Toxic Substances and Disease Registry ...

MERCURY 112
2. HEALTH EFFECTS
Groups of 10 female Sprague-Dawley rats were administered a single gavage dose of mercuric chloride at
7.4 or 9.2 mg Hg/kg in water and necropsied at 14 days postexposure. There were no effects on body or
relative liver weights from mercuric chloride exposure. LDH activity was significantly decreased in
animals exposed to HgCl2 at both dose levels. Mercury was found mainly in the kidneys (12.6 and
18.9 ppm at the low and high dose, respectively), but trace amounts were also detected in the liver, brain,
and serum (Lecavalier et al. 1994).
Two intermediate-duration studies in rats showed biochemical changes following ingestion of mercuric
chloride (Jonker et al. 1993b; Rana and Boora 1992). Increases in hepatic lipid peroxidation and decreases
in glutathione peroxidase were observed in rats orally exposed to an unspecified dose of mercuric chloride
for 30 days (Rana and Boora 1992). In a 4-week range-finding study, groups of 5 rats per sex (10 per sex
for controls) received diets containing mercuric chloride at 5, 10, or 20 mg Hg/kg/day in males and 5.5,
11.1, and 22.2 mg Hg/kg/day in females. Absolute liver weight decreased starting at the mid-dose group in
males and in the high-dose group in females (Jonker et al. 1993b). The liver weight significantly increased
in mice given 2.9 mg Hg/kg/day as mercuric chloride in the drinking water for 7 weeks; however, no
histopathological changes were observed (Dieter et al. 1983). Male rats administered mercuric chloride by
gavage for 2 years showed a slight increase in acute hepatic necrosis (11 of 50 versus 4 of 50 in controls);
however, it is unclear whether this increase was statistically significant (NTP 1993).
Organic Mercury. Extremely limited information was also obtained regarding the hepatic effects of
organic mercury exposure. An autopsy of four adults and four infants who died as the result of methyl­
mercury poisoning in Iraq in 1972 reported fatty changes in the liver occurred in most cases (Al-Saleem and
the Clinical Committee on Mercury Poisoning 1976). It is unclear whether these changes were the direct
result of methylmercury on the liver or whether they were due to other causes. The prevalence of liver
disease in a population from the Minamata area was not significantly increased when compared to
unexposed controls (Futatsuka et al. 1992).
No treatment-related changes were observed in hepatic parameters measured in rats exposed via the diet to
0.1 mg Hg/kg/day as methylmercuric chloride (Verschuuren et al. 1976).