Page 493 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

460 SECTION | V Metals and Micronutrients

VetBooks.ir for 2 weeks (NTP, 1993). In a 2-year gavage study, an with the use of chelators, along with protein solutions to
bind and neutralize mercury compounds. The use of a par-
increased incidence of forestomach hyperplasia was
ticular chelator is dependent upon the type of mercury
observed in male rats exposed to 1.9 or 3.7 mg Hg/kg/day
as mercuric chloride compared to the control group. Mice exposure. Among several chelators, dimercaprol (BAL,
showed ulceration of the glandular stomach after 2 years 3 mg/kg, im) has been found to be the most effective
of dietary exposure to methylmercuric chloride at 0.69 mg against mercury poisoning. However, chelation releases
Hg/kg/day (Mitsumori et al., 1981, 1990). mercury from soft tissues which can be redistributed to the
brain. Oral administration of sodium thiosulfate (1 g/kg)
can assist in eliminating mercury. Recently, Takemoto
Hematopoietic System
et al. (2015) mentioned that living animals are equipped
In general, acute mercury toxicity does not produce any with a set of endogenous defense mechanisms against Hg,
characteristic hematological changes. In a chronic study such as vitamin E, vitamin K, selenium, metallothioneine,
conducted in rats, phenylmercuric acetate given in water 17B-estradiol, and brain derived neurotrophic factor.
at a dose of 4.2 mg Hg/kg/day caused decreases in hemo- Animal studies suggest that antioxidants (particularly vita-
globin, hematocrit and RBC counts (Solecki et al., 1991). min E) may be useful for decreasing the toxicity of mer-
The anemia observed in this study may have been second- cury. Improved chelation and drug therapies for treating
ary to blood loss associated with the ulcerative lesions in acute and chronic mercury poisonings are greatly needed.
the large intestine. However, methylmercuric chloride at a
low dose (0.1 mg Hg/kg/day for 2 years) given in the diet
for 2 years caused no changes in hematological para- CONCLUDING REMARKS AND FUTURE
meters (Verschuuren et al., 1976).
DIRECTIONS
Other Effects Toxicity by mercury depends upon the form of mercury,
dose, duration and route of exposure. Organic mercury
Mercury has been found to have the potential for inducing tends to bioaccumulate in the higher food chain, and as a
genotoxicity (Ghosh et al., 1991), carcinogenicity (Solecki result the maximum concentrations are found in the meat
et al., 1991; NTP, 1993), immunotoxicity (Thuvander of fish, marine mammals and fish-eating birds and wild-
et al., 1996), and endocrine, reproductive and developmen- life. Methylmercury is the most toxic among the mercury
tal toxicity (Fuyuta et al., 1979; Castoldi et al., 2008; species because of its volatility and its ability to pass
Liang et al., 2009; Tan et al., 2009; Vitalone et al., 2010; through biological membranes such as the BBB and the
Liso ´n et al., 2016; Ni et al., 2017). placental barrier. The nervous system and kidneys are the
two major target organs. Not all forms of mercury cross
DIAGNOSIS the BBB (e.g., inorganic mercury), but in all forms it
accumulates in the kidney and thereby causes damage to
Presently there are reliable and accurate ways to measure this organ. Chelation therapy appears to be the best treat-
mercury levels in the body, using an atomic absorption ment. Oral administration of activated charcoal is very
spectrometer and inductively coupled plasma (ICP) or effective in reducing the further absorption of mercury
ICP-mass spectrometer (ICP-MS). Mercury analysis is from the GI tract.
usually performed on blood, urine, milk, hair, nail, liver,
and kidney. Mercury in urine is determined to test for
exposure to metallic or inorganic mercury, while whole REFERENCES
blood or hair values are used to determine exposure to
methylmercury. Mercury levels in the blood provide more Al-Saleem, T., 1976. Levels of mercury and pathologic changes in
useful information after recent exposures than after long- patients with organomercury poisoning. Bull. World Health Org. 53
term exposures. Levels found in blood, urine and hair may (Suppl.), 99 104.
be used together to predict possible health effects that may Arito, H., Takahashi, M., 1991. Effect of methylmercury on sleep pat-
terns in the rat. In: Suzuki, T., Imura, N., Clarkson, T.W. (Eds.),
be caused by the different forms of mercury. The kidney is
Advances in Mercury Toxicology. Plenum Press, New York, NY,
an ideal specimen for mercury analysis from dead animals.
pp. 381 394.
Ashe, W., Largent, E., Dutra, F., et al., 1953. Behaviour of mercury in
TREATMENT the animal organism following inhalation. Arch. Ind. Hyg. Occup.
Med. 17, 19 43.
Activated charcoal (1 3 g/kg body weight, po) is very ATSDR, Agency for Toxic Substances and Disease Registry, 1999.
effective in reducing further absorption of mercury from Toxicological Profile for Mercury. U.S. Department of Health and
the GI tract. Specific treatment of mercury poisoning rests Human Services, Atlanta, GA.