Evaluation of Clastogenic/Aneugenic Damage Using the FISH Micronucleus Assay in Mice Exposed to Chromium (VI).

Background/aim: Exposure to chromium (VI) [Cr(VI)] has been postulated to be associated with the induction of cancer. In vivo studies utilizing biomarkers of genotoxic damage could aid in elucidating the mechanisms underlying the genotoxic effects of Cr(VI) and their relationship with carcinogenesis. In this study, the origin (clastogenic and/or aneugenic damage) and kinetics of micronuclei (MN) induced by Cr(VI) were investigated.

Vanadium(IV) oxide affects embryonic development in mice.

Vanadium(V) and vanadium(IV) are the predominant redox forms present in the environment, and epidemiological studies have reported that prenatal vanadium exposure is associated with restricted fetal growth and adverse birth outcomes. However, data about the toxic effects of vanadium(IV) oxide (V O ) on the development of mammals are still limited. Therefore, in this work, 4.

Vanadium oxides modify the expression levels of the p21, p53, and Cdc25C proteins in human lymphocytes treated in vitro.

In vitro assays have demonstrated that vanadium compounds interact with biological molecules similar to protein kinases and phosphatases and have also shown that vanadium oxides decrease the proliferation of cells, including human lymphocytes; however, the mechanism, the phase in which the cell cycle is delayed and the proteins involved in this process are unknown. Therefore, we evaluated the effects of vanadium oxides (V O , V O and V O ) in human lymphocyte cultures (concentrations of 2, 4, 8, or 16 μg/ml) on cellular proliferation and the levels of the p53, p21 and Cdc25C proteins. After 24 h of treatment with the different concentrations of vanadium oxides, the cell cycle phases were determined by evaluating the DNA content using flow cytometry, and the levels of the p21, p53 and Cdc25C proteins were assessed by Western blot analysis.

Antigenotoxic effects of (-)-epigallocatechin-3-gallate (EGCG) and its relationship with the endogenous antioxidant system, 8-hydroxydeoxyguanosine adduct repair (8-OHdG), and apoptosis in mice exposed to chromium(VI).

This study aimed to investigate the relationship between endogenous antioxidant system, 8-hydroxydeoxyguanosine adduct (8-OHdG) repair, and apoptosis in mice treated with chromium(VI) alone and in the presence of the antigenotoxic compound (-)-epigallocatechin-3-gallate (EGCG). Groups of 5 Hsd:ICR male mice were divided and treated as follows: (1) control, vehicle only; (2) EGCG, 8.5 mg/kg by gavage alone; (3) CrO, 20 mg/kg intraperitoneally alone; and (4) EGCG combined with CrO, EGCG was administered 4 hr prior to CrO.

Effect on the offspring of pregnant females CD-1 mice treated with a single thallium(I) application.

Thallium (Tl) is a highly toxic metal for human beings; higher amounts found in diverse fluids of pregnant women are associated with low birth weight and preterm birth. However, experimental data concerning their effects on the embryonic development of mammalian organisms are limited. Hence, in the present work, TI(I) acetate of 0, 4.

Premature chromatid separation and altered proliferation of human leukocytes treated with vanadium (III) oxide.

Vanadium is a widely distributed metal in the Earth's surface and is released into the environment by either natural or anthropogenic causes. Vanadium (III) oxide (VO) is present in the environment, and many organisms are exposed to this compound; however, its effects at the cellular and genetic levels are still unknown. Therefore, in this study, the ability of VO to induce chromosomal damage and impair cell proliferation was tested on human leukocytes in vitro.

Genotoxicity of Casiopeina III-Ea in mouse bone marrow cells.

Casiopeina III-Ea® (Cas III-Ea®) is a chelated copper complex with antineoplastic activity that is capable of reducing tumor size and inducing antiproliferative and apoptotic effects. However, little is known about its in vivo genotoxic effects. Therefore, this study evaluated two cytogenetic and two proliferative parameters 24 h after the administration of Casiopeina III-Ea® to male CD-1 mice.

In Vivo Effects of Vanadium Pentoxide and Antioxidants (Ascorbic Acid and Alpha-Tocopherol) on Apoptotic, Cytotoxic, and Genotoxic Damage in Peripheral Blood of Mice.

This study was conducted to investigate the effects of vanadium pentoxide (V2O5), ascorbic acid (AA), and alpha-tocopherol (α-TOH) on apoptotic, cytotoxic, and genotoxic activity. Groups of five Hsd:ICR mice were treated with the following: (a) vehicle, distilled water; (b) vehicle, corn oil; (c) AA, 100 mg/kg intraperitoneally (ip); (d) α-TOH, 20 mg/kg by gavage; (e) V2O5, 40 mg/kg by ip injection; (f) AA + V2O5; and (g) α-TOH + V2O5. Genotoxic damage was evaluated by examining micronucleated polychromatic erythrocytes (MN-PCE) obtained from the caudal vein at 0, 24, 48, and 72 h after treatments.

In vitro DNA damage by Casiopeina II-gly in human blood cells.

A variety of metal ions have biological functions, and many researchers have not actively investigated copper compounds, based on the assumption that endogenous metals might be less toxic. In the present study, we used a dual fluorochrome method and a single cell gel electrophoresis (SCGE) assay at pH > 13 to evaluate the cell viability and DNA damage induced by a copper-based antineoplastic drug, Casiopeina II-gly®, at concentrations of 1.04, 2.

Modulation of hexavalent chromium-induced genotoxic damage in peripheral blood of mice by epigallocatechin-3-gallate (EGCG) and its relationship to the apoptotic activity.

This study was conducted to investigate the relationship between modulation of genotoxic damage and apoptotic activity in Hsd:ICR male mice treated with (-)-epigallocatechin-3-gallate (EGCG) and hexavalent chromium [Cr(VI)]. Four groups of 5 mice each were treated with (i) control vehicle only, (ii) EGCG (10 mg/kg) by gavage, (iii) Cr(VI) (20 mg/kg of CrO3) intraperitoneally (ip), and (iv) EGCG in addition to CrO3 (EGCG-CrO3). Genotoxic damage was evaluated by examining presence of micronucleated polychromatic erythrocytes (MN-PCE) obtained from peripheral blood of the caudal vein at 0, 24, 48, and 72 h after treatment.

[IN VIVO EFFECT OF RED WINE UNDILUTED, DILUTED (75%) AND ALCOHOL-FREE ON THE GENOTOXIC DAMAGE INDUCED BY POTENTIAL CARCINOGENIC METALS: CHROMIUM [VI]].

Introduction: the carcinogenesis may be initiated and promoted by the oxidative DNA damage. The compounds of chrome (Cr [VI]) cause oxidative stress (EOx) and are recognized as carcinogens in humans. In this sense, it is proposed that drinks with a high antioxidative potential, such as red wine, may have protective or modulatory effects on the oxidative DNA damage.

Hydroxyurea induces chromosomal damage in G2 and enhances the clastogenic effect of mitomycin C in Fanconi anemia cells.

Fanconi's anemia (FA) is a recessive disease; 16 genes are currently recognized in FA. FA proteins participate in the FA/BRCA pathway that plays a crucial role in the repair of DNA damage induced by crosslinking compounds. Hydroxyurea (HU) is an agent that induces replicative stress by inhibiting ribonucleotide reductase (RNR), which synthesizes deoxyribonucleotide triphosphates (dNTPs) necessary for DNA replication and repair.

Antigenotoxic effects of (-)-epigallocatechin-3-gallate (EGCG), quercetin, and rutin on chromium trioxide-induced micronuclei in the polychromatic erythrocytes of mouse peripheral blood.

This study was conducted to investigate the modulating effects of (-)-epigallocatechin-3-gallate (EGCG), quercetin, and rutin on the genotoxic damage induced by Cr(VI) in polychromatic erythrocytes of CD-1 mice. The animals were divided into the following groups: (i) vehicle only; (ii) flavonoids (10 mg/kg EGCG, 100 mg/kg quercetin, 625 mg/kg rutin, or 100-625 mg/kg quercetin-rutin); (iii) Cr(VI) (20 mg/kg of CrO3); and (iv) flavonoids concomitantly with Cr(VI). All of the treatments were administered intraperitoneally (i.

Antigenotoxic and apoptotic activity of green tea polyphenol extracts on hexavalent chromium-induced DNA damage in peripheral blood of CD-1 mice: analysis with differential acridine orange/ethidium bromide staining.

This study was conducted to investigate the modulating effects of green tea polyphenols on genotoxic damage and apoptotic activity induced by hexavalent chromium [Cr (VI)] in CD-1 mice. Animals were divided into the following groups: (i) injected with vehicle; (ii) treated with green tea polyphenols (30 mg/kg) via gavage; (iii) injected with CrO3 (20 mg/kg) intraperitoneally; (iv) treated with green tea polyphenols in addition to CrO3. Genotoxic damage was evaluated by examining micronucleated polychromatic erythrocytes (MN-PCEs) obtained from peripheral blood at 0, 24, 48, and 72 h after treatment.

Evaluation of cytogenetic and DNA damage caused by thallium(I) acetate in human blood cells.

Although thallium is detrimental to all living organisms, information regarding the mutagenic and genotoxic effects of this element and its compounds remains scarce. Therefore, we tested the genotoxic and cytotoxic effects of thallium(I) acetate on human peripheral blood cells in vitro using structural chromosomal aberrations (SCAs), sister chromatid exchanges (SCEs), and single-cell gel electrophoresis (at pH >13 or 12.1) analysis.

Sex differences in blood genotoxic and cytotoxic effects as a consequence of vanadium inhalation: micronucleus assay evaluation.

Vanadium is an environmental pollutant attached to the smallest air suspended particles that enters into the respiratory tract reaching the systemic circulation. The oxidative state of this element and sex are factors related to its toxicity. In this study, we explored sex-associated genotoxic and cytotoxic differences in a mouse experimental model.

Genetic toxicology of thallium: a review.

This review summarizes the current knowledge about the general toxicity of thallium (Tl) and its environmental sources, with special emphasis placed on its potential mutagenic, genotoxic, and cytotoxic effects on both eukaryotic and prokaryotic cells. Tl is a nonessential heavy metal that poses environmental and occupational threats as well as therapeutic hazards because of its use in medicine. It is found in two oxidation states, thallous (Tl(+)) and thallic (Tl(3+)), both of which are considered highly toxic to human beings and domestic and wild organisms.

Hepatic megalocytosis due to vanadium inhalation: participation of oxidative stress.

The aim of this study was to evaluate the morphological changes, liver function test (LFT), and oxidative stress damage caused by thiobarbituric acid reactive substances (TBARS), in mice exposed to vanadium via inhalation. Male CD-1 mice were exposed to vanadium pentoxide (V(2)O(5)) via inhalation (0.02 M), 1 hour twice a week for 6 weeks.

DNA damage induction in human cells exposed to vanadium oxides in vitro.

Vanadium and vanadium salts cause genotoxicity and elicit variable biological effects depending on several factors. In the present study, we analyzed and compared the DNA damage and repair processes induced by vanadium in three oxidation states. We used human blood leukocytes in vitro and in a single cell gel electrophoresis assay at two pH values.

Age-related sex differences in glutathione peroxidase and oxidative DNA damage in a healthy Mexican population.

Background And Objective: It has been proposed that women have an estrogen activity-linked biological antioxidant advantage and that this advantage is lost in the postmenopausal stage. The latter remains controversial. Our aim was to determine age-related sex differences in oxidative stress and oxidative DNA damage in a healthy Mexican population.

Chromosomal damage induced by vanadium oxides in human peripheral lymphocytes.

Fly ash, the inorganic residue resulting from the combustion of some fuels, may almost exclusively contain vanadium oxides, compounds which exert potential toxic effects on a wide variety of in vitro and in vivo biological systems. Because information related to the oxidation state responsible for inducing genotoxic effects is controversial, the aim of the present study was to evaluate the effects of three vanadium salts in vitro. Human peripheral lymphocyte cultures were exposed to 1, 2, 4, or 8 microg/mL of vanadium(III) trioxide, vanadium(IV) tetraoxide, or vanadium(V) pentoxide (V(2)O(3), V(2)O(4), or V(2)O(5), respectively).

In vitro effect of malathion and diazinon on oocytes fertilization and embryo development in porcine.

Diazinon and malathion are commonly used organophosphate insecticides in agriculture, industry, and in veterinary medicine as an ectoparasiticide. The importance to carry out in vitro reproductive toxicology assays lies on the need of knowing the alterations these insecticides may cause at cellular level, since they are endocrine disruptors that interfere with reproductive functions. The aim of this study was to evaluate in vitro oocyte viability, fertilization, and embryo development with different concentrations of diazinon and malathion.

High dosage of ascorbic acid and alpha-tocopherol is not useful for diminishing oxidative stress and DNA damage in healthy elderly adults.

Aim: To determine the useful dosage of ascorbic acid and alpha-tocopherol against oxidative stress and DNA damage in the elderly.

Methods: A double-blind controlled clinical assay carried out in a sample of 66 healthy subjects divided into three age-paired random groups with 22 subjects in each group. Group A received placebo and group B was administered 500 mg of ascorbic acid and 400 IU of alpha-tocopherol, whereas group C received 1,000 mg of ascorbic acid and 400 IU of alpha-tocopherol for a 6-month period.