Chinese hamster cells toxicity

Ishidate, M., Jr Odashima, S. (1977) Chromosome tests with 134 compounds on Chinese hamster cells in vitro—a screening for chemical carcinogens. Mutat. Res., 48, 337-354 Izmerov, N. F. (1984) Pyridine (IRPTC Scientific Reviews of Soviet Literature on Toxicity and Hazards of Chemicals), United Nations Environmental Programme, Moscow, Centre of International Projects, GKNT... 

Jansson, K. Jansson, V. (1993) The toxicity of chlorophenols in V79 Chinese hamster cells. Toxicol. Lett., 69, 289-294... 

Ishidate M. Jr., Yoshikawa K. 1980. Chromosome aberration tests with Chinese hamster cells in vitro with and without metabolic activation A comparative study on mutagens and carcinogens. In Further studies in the assessment of toxic actions. Arch Toxicol Suppl 4 41-44. 

Cleaver JE (1984) Differential toxicity of 3-aminobenzamide to wild-type and 6-thioguanine-resistant Chinese hamster cells by interference with pathways of purine biosynthesis. Mutat Res 131 123-127... 

Trp-P-2 and IQ have been evaluated in a repair-deficient Chinese hamster cell forward mutation system (Thompson et al., 1983). Trp-P-2 was very potent for producing mutations at both the hprt and aprt loci in both the repair competent AA8 cell line and the repair incompetent UV-5 line (see figure 1). In contrast to these results, IQ was quite weak. Equivalent mutation and toxicity effects were seen only at doses of IQ that were 70-100 fold higher than used for Trp-P-2. With IQ, toxicity differences were seen between the repair proficient and deficient strains. These results indicate that some of the damage leading to toxicity produced by IQ is not repairable by the excision repair pathway. Also, only the repair deficient strain showed a mutagenic response. Thus, in contrast to Salmonella, the CHO cells are much more responsive to Trp-P-2 than to IQ. 

Scand J Work Environ Health 12 523-537 Oberddrster G, Cox C (1990) Carcinogenicity of cadmium in animals what is the significance for man Chem Environ Toxicol 27 181-195 Ochi T, Ishiguro T, Ohsawa M (1983) Participation of active oxygen species in the induction of DNA single-strand scissions by cadmium chloride in cultured Chinese hamster cells. Mutat Res 122 169-175 Ochi T, Otsuka F, Takahashi K, Ohsawa M (1988) Glutathione and metallothioneins as cellular defense against cadmium toxicity in cultured Chinese hamster cells. Chem Biol Interact 65 1-14... 

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. 

Crosby, D.G. and R.K. Tucker. 1966. Toxicity of aquatic herbicides to Daphniamagna. Science 154 289-291. Darr, D.J., S. Yanni, and S.R. Pinnell. 1988. Protection of Chinese hamster ovary cells from paraquat-mediated cytotoxicity by a low molecular weight mimic of superoxide dismutase (DF-Mn). Free Radical Biol. Med. 4 357-363. 

The use of triphenylethylene SERMs as Pgp inhibitors for clinical application has been hampered by unacceptable toxicity at doses required to achieve adequate cellular concentration, which is likely due to the involvement of proteins with the ability to bind these compounds. For instance, toremifene is able to reverse MDR and to sensitize human renal cancer cells to vinblastine in vitro. However, in vivo toremifene is tightly bound to serum proteins, in particular a 1-acid glycoprotein (AAG), which may limit its tissue availability (Braybrooke et al. 2000). In agreement with this, Chatterjee and Harris (1990) have shown that tamoxifen and 4-OH-tamoxifen were similarly potent in reversing MDR in Chinese hamster ovary (CHO) cells with acquired resistance to adriamycin. However, the addition of AAG (0.5 to 2 mg/ml, the range found in vivo) to cell cultures decreased the effect of tamoxifen on reversing MDR, and at the highest AAG concentration there was a complete reversal of the effects of... 

Garrett NE, Lewtas J. 1983. Cellular toxicity in Chinese hamster ovary cell cultures I. Analysis of cytotoxicity endpoints for twenty-nine priority pollutants. Environ Res 32 455-465. 

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