Chromium (VI)-induced DNA damage in chick embryo liver and blood cells in vivo

Currently we are faced with an ever-growing use of Δ9-tetrahydrocannabinol (THC) preparations, often used as supportive therapies for various malignancies and neurological disorders. As some of illegally distributed forms of such preparations, like cannabis oils and butane hash oil, might contain over 80% of THC, their consumers can become intoxicated or experience various detrimental effects. This fact motivated us for the assessments of THC toxicity in vivo on a Wistar rat model, at a daily oral dose of 7 mg/kg which is comparable to those found in illicit preparations. The main objective of the present study was to establish the magnitude and dynamics of DNA breakage associated with THC exposure in white blood and brain cells of treated rats using the alkaline comet assay. The extent of oxidative stress after acute 24 h exposure to THC was also determined as well as changes in activities of plasma and brain cholinesterases (ChE) in THC-treated and control rats. The DNA of brain cells was more prone to breakage after THC treatment compared to DNA in white blood cells. Even though DNA damage quantified by the alkaline comet assay is subject to repair, its elevated level detected in the brain cells of THC-treated rats was reason for concern. Since neurons do not proliferate, increased levels of DNA damage present threats to these cells in terms of both viability and genome stability, while inefficient DNA repair might lead to their progressive loss. The present study contributes to existing knowledge with evidence that acute exposure to a high THC dose led to low-level DNA damage in white blood cells and brain cells of rats and induced oxidative stress in brain, but did not disturb ChE activities.

Download Full-text

The effects of chemical carcinogens on hormone-inducible gene expression in chick embryo liver in vivo.

10.1349/ddlp.3256 ◽

1994 ◽

Author(s):

Jennifer McCaffrey

Keyword(s):

Gene Expression ◽

Chick Embryo ◽

Chemical Carcinogens ◽

Inducible Gene Expression ◽

Embryo Liver ◽

Inducible Gene

Download Full-text

Effects of porphyrin-inducing drugs on ferrochelatase activity in isolated mouse hepatocytes

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y81-178 ◽

1981 ◽

Vol 59 (11) ◽

pp. 1155-1158 ◽

Cited By ~ 5

Author(s):

Susan P. C. Cole ◽

Thomas E. Massey ◽

Gerald S. Marks ◽

William J. Racz

Keyword(s):

Cell Culture ◽

Chick Embryo ◽

Liver Cell ◽

Mouse Hepatocyte ◽

Liver Cell Culture ◽

Embryo Liver ◽

Mouse Hepatocytes ◽

The Difference ◽

Hepatocyte Suspension

The effects of several concentrations of griseofulvin and 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine (DDC) on ferrochelatase activity in suspensions of isolated mouse hepatocytes were examined. In agreement with previous findings in the intact chick embryo liver and chick embryo liver cell culture, DDC, but not griseofulvin, inhibited the enzyme in the isolated mouse hepatocyte suspension. These results indicate that the difference between the effects of griseofulvin on hepatic ferrochelatase in rodents in vivo (inhibition), the intact chick embryo (no effect), and the chick embryo liver cell culture (no effect) cannot be attributed solely to species differences.

Download Full-text

E.P.R. Spectroscopic Studies of the Reactions of Chromium(VI) with L-Ascorbic Acid in Buffer Solutions: Implications for Understanding the Roles of Chromium(V) and Chromium(IV) Species and the Buffer Dependences of In Vitro DNA Damage

Australian Journal of Chemistry ◽

10.1071/ch00005 ◽

2000 ◽

Vol 53 (1) ◽

pp. 7 ◽

Cited By ~ 10

Author(s):

Lianbo Zhang ◽

Peter A. Lay

Keyword(s):

Dna Damage ◽

Ascorbic Acid ◽

Spectroscopic Studies ◽

Mixed Ligand ◽

Peroxo Complexes ◽

Buffer Solutions ◽

Chromium Vi ◽

Dna Strand

The reaction of chromium(VI) with L-ascorbic acid (AsA) in buffer solutions was investigated by e.p.r. spectroscopy. Chromium(V)/ascorbate complexes with signals at giso = 1.9791 and chromium(VI)/ascorbate/peroxo complexes with signals at giso = 1.9819 and giso = 1.9824 were observed in all buffers. New signals at giso values of 1.9765 and 1.9781 were observed in Tris–HCl [tris(hydroxymethyl)aminomethane hydrochloride] buffer and were assigned to a mixed-ligand ascorbate/Tris complex of chromium(V), [CrO(ascorbate)(Tris)]2– , and a Tris/peroxo species, [CrO(O2)(Tris)]2– , respectively. The speciation of the e.p.r.-active chromium(V) complexes detected from solutions with other buffers, such as HEPES, cacodylate and phosphate, was not influenced by the buffer type. Preincubation of catalase with ascorbate solutions inhibited the formation of the chromium(V) peroxo species in all buffers. Manganese(II) reduces the chromium(V) species produced in the reaction, which has shown that it is inappropriate to use manganeses(II) as a selective reagent for monitoring the concentrations of chromium(IV) in such reactions. In particular, manganeses(II) reacts more efficiently with the chromium(V) species that are most damaging to DNA in vitro, viz., the mixed-ligand chromium(V)/ascorbate/peroxo complexes. The correlation of the present results with those of in vitro DNA damage experiments reported in the literature has revealed that the chromium(V)/ascorbate/peroxo species are the major species responsible for the in vitro DNA strand breaks in all of the buffer systems. These species are not expected to be as important in vivo.

Download Full-text