Lead genotoxicity

It is well known that excessive intake of P-carotene may lead to carotenodermia (yellow skin), and it is undoubtedly the case that some carotenoid is directly lost via the skin or through photo-oxidation in the skin. As far as is known the carotenoids are not cytotoxic or genotoxic even at concentrations up to 10 times the normal plasma concentration which may cause carotenodermia. However, they are associated with amenorrhoea in girls who may be consuming bizarre diets and, in long-term supplementation studies, with an increase in lung cancer (The Alpha-tocopherol, Beta-carotene Cancer Prevention Study Group, 1994). 

Kinetic Constants and Model Parameters in the O Flaherty Model 2-7 Residence Times in the Biokinetic Module of the IEUBK Model 2-8 Kinetic Constants and Model Parameters in the Leggett Model 2-9 Summary of Blood Slope Factors from Various Environmental Media 2-10 Genotoxicity of Lead In Vivo 2-11 Genotoxicity of Lead In Vitro... 

No studies were located regarding genotoxic effects in humans or animals after inhalation exposure to inorganic lead. See Section 2.2.1.7 for a discussion of these effects in humans after multi-route exposure to inorganic lead. 

Genotoxic Effects. Evaluation of the genotoxicity of lead in humans has focused on evaluations of lymphocytes from occupationally or environmentally exposed persons (Table 2-10) and in vitro studies of structural chromosomal aberrations and sister chromatid exchange in cultures of lymphocytes taken from healthy individuals (Table 2-11). Results of studies with human lymphocyte cultures exposed in vitro to lead acetate were nearly equally divided between positive (Beek and Obe 1974 Niebuhr and Wulf 1984) and negative (Beek and Obe 1975 Deknudt and Deminatti 1978 Gasiorek and Bauchinger 1981 Schmid etal. 1972). 

A single intracardiac dose of 40 ig/g body weight lead acetate induced a 25-fold increase in mitosis of mouse liver cells 5 hours after injection (Choie and Richter 1978). Results were mixed for various manifestations of genotoxicity or cell cycle disruptions in several experiments with lead acetate in mammals (Bruce and Heddle 1979 Deknudt and Gerber 1979 Deknudt et al. 1977 Jacquet and Tachon 1981 Jacquet et al. 1977 Muro and Goyer 1969 Tachi et al. 1985 Willems et al. 1982). 

Cerklewski and Forbes 1976). Also, excess zinc protects zinc-containing enzymes like ALAS, ferrochelatase, and ALAD. In vivo, aqueous solution containing zinc administered to rats significantly reduced the genotoxic effects induced by lead (Kowalska-Wochna et al. 1988). It was postulated that zinc s protective action may be related to its functioning in DNA and RNA polymerases and consequent enhancement of cell repair processes. 

Hartwig A. Schlepegrell R. Beyersmann D. 1990. Indirect mechanism of lead-induced genotoxicity in cultured mammalian cells. Mutat Res 241 75-82. 

Kharab P, Singh I. 1985. Genotoxic effects of potassium dichromate, sodium arsenite, cobalt chloride and lead nitrate in diploid yeast. MutRes 155 117-120. 

Nayak BN, Ray M, Persaud TVN. 1989b. Relationship of embryotoxicity to genotoxicity of lead nitrate in mice. Exp Pathol 36 65-73. 

Niebuhr E, Wulf HC. 1984. Chapter 9 Genotoxic Effects. In Grandjean P, ed. Biological effects of organo-lead compounds. Boca Raton, FL CRC Press, 117-124. 

DNA effects Damage to DNA (Deoxyribonucleic acid) by a chemical or material may result in genotoxic effects such as mutations, which in turn may lead to carcinogenicity. Damage to DNA causes the cell to manufacture new DNA to compensate for the loss or damage. This can be assessed by evaluating the formation of newly synthesized DNA. Unscheduled DNA Synthesis... 

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