DNA Damage In Group Research Articles

Protective Effects of Taurine on Imidacloprid-Induced DNA Damage and Reproductive Performance in The Drosophila melanogaster Model

Imidacloprid is a neonicotinoid group insecticide and is widely used in veterinary medicine for the control of pests such as lice and fleas in domestic animals. Insecticides are known that they induce toxic effects on living organism, causing oxidative stress and DNA damage. Taurine plays a role in many physiological and biochemical functions and provides an antioxidant effect by stabilization of biological membranes. This study investigated the effect of imidacloprid on DNA damage and reproductive performance and the possible protective effect of taurine in Drosophila melanogasters. Imidacloprid (0.6 µM) alone or in combination with taurine (1, 2 ve 3 mM) were given to broths for 20 days. The results of the study showed that imidacloprid application decreased reproductive performance and increased DNA damage in groups, whereas these effects decreased with taurine administration. In conclusion, it was determined that the adverse effects of imidacloprid regarding DNA and reproductive performance in Drosophila melanogasters were prevented by taurine application.

Toxicological analysis and anti-inflammatory effects of essential oil from Piper vicosanum leaves

This study assessed the anti-inflammatory effects of the essential oil from Piper vicosanum leaves (OPV) and evaluated the toxicological potential of this oil through acute toxicity, genotoxicity and mutagenicity tests. The acute toxicity of OPV was evaluated following oral administration to female rats at a single dose of 2 g/kg b.w. To evaluate the genotoxic and mutagenic potential, male mice were divided into five groups: I: negative control; II: positive control; III: 500 mg/kg of OPV; IV: 1000 mg/kg of OPV; V: 2000 mg/kg of OPV. The anti-inflammatory activity of OPV was evaluated in carrageenan-induced pleurisy and paw edema models in rats. No signs of acute toxicity were observed, indicating that the LD50 of this oil is greater than 2000 mg/kg. In the comet assay, OPV did not increase the frequency or rate of DNA damage in groups treated with any of the doses assessed compared to that in the negative control group. In the micronucleus test, the animals treated did not exhibit any cytotoxic or genotoxic changes in peripheral blood erythrocytes. OPV (100 and 300 mg/kg) significantly reduced edema formation and inhibited leukocyte migration analyzed in the carrageenan-induced edema and pleurisy models. These results show that OPV has anti-inflammatory potential without causing acute toxicity or genotoxicity.

Assessment of the cytotoxic, genotoxic, and mutagenic potential of Acrocomia aculeata in rats.

Acrocomia aculeata (Jacq.) Lodd. ex Mart. is a plant species commonly used as a foodstuff and also for treating diseases, since it contains high concentrations of antioxidant compounds and monounsaturated fatty acids. Considering its ethnopharmacological relevance, the aim of the present study was to assess the cytotoxic, genotoxic, and mutagenic effects of an oil extracted from the pulp of A. aculeata (OPAC) in rats. In addition, a chromatographic characterization of the fatty acids present in OPAC was performed. Male and female Wistar rats were treated orally with 125, 250, 500, 1000, or 2000 mg/kg/body weight OPAC. The effects of OPAC ingestion were determined by performing the comet assay and micronucleus test. The comet assay data demonstrated that OPAC did not increase the frequency or rate of DNA damage in groups treated with any of the concentrations assessed compared to that in the negative control group. In the micronucleus test, the animals treated did not exhibit any cytotoxic or mutagenic changes in peripheral blood erythrocytes. The results demonstrated that OPAC did not exhibit cytotoxic, genotoxic, or mutagenic effects in Wistar rats, thereby increasing the evidence for the safety of oil extracted from this plant.

Genotoxic effects of the herbicide Roundup® in the fish Corydoras paleatus (Jenyns 1842) after short-term, environmentally low concentration exposure

The glyphosate-based herbicide, Roundup(®), is one of the most used pesticides worldwide. In concert with the advent of transgenic crops resistant to glyphosate, the use of this pesticide has led to an increase in agricultural yields. The objective of this study was to evaluate the genotoxic effect that the herbicide Roundup(®) (at a concentration of 6.67μg/L, corresponding to 3.20μg/L glyphosate) can have on the fish Corydoras paleatus. Treatment groups were exposed for 3, 6, and 9days, and effects were analyzed using the piscine micronucleus test (PMT) and comet assay. A group subjected to filtered water only was used as a negative control. The PMT did not show differences between the control and exposed groups for any of the treatment times. In contrast, the comet assay showed a high rate of DNA damage in group exposed to Roundup(®) for all treatment times, both for blood and hepatic cells. We conclude that for the low concentration used in this research, the herbicide shows potential genotoxic effects. Future research will be important in evaluating the effects of this substance, whose presence in the environment is ever-increasing.

Potential role of melatonin in DNA damage caused by nitrosourea-induced mammary carcinogenesis

Mammary carcinogenesis was induced in female Sprague-Dawley rats by exposure to N-methyl-N-nitrosourea (NMU). Animals were kept under constant light conditions to arrest endogenous melatonin synthesis and were fed the same melatonin dosage, since nitrosourea exposure may also induce cellular injury, especially with extensive proliferative activity. The pro-apoptotic effects of the biogenic amine, melatonin, on rat whole blood leukocytes were assessed by alkaline single cell gel electrophoresis (comet) assay. Potential induction of stress due to animal immobilization and its additional effect on DNA damage was studied. The parameters relevant to the degree of DNA damage in groups with chemocarcinogen treatment demonstrated no significant effects as a result of the immobilization. A significant increase in DNA damage after melatonin treatment in NMU-induced carcinogenesis confirms its involvement in the activation of apoptosis.

Influence of a static magnetic field (250 mT) on the antioxidant response and DNA integrity in THP1 cells

The aim of this study was to investigate the effect of static magnetic field (SMF) exposure in antioxidant enzyme activity, the labile zinc fraction and DNA damage in THP1 cells (monocyte line). Cell culture flasks were exposed to SMF (250 mT) during 1 h (group 1), 2 h (group 2) and 3 h (group 3). Our results showed that cell viability was slightly lower in SMF-exposed groups compared to a sham exposed group. However, SMF exposure failed to alter malondialdehyde (MDA) concentration (+6%, p > 0.05) and glutathione peroxidase (GPx) (−5%, p > 0.05), catalase (CAT) (−6%, p > 0.05) and superoxide dismutase (SOD) activities (+38%, p > 0.05) in group 3 compared to the sham exposed group. DNA analysis by single cell gel electrophoresis (comet assay) revealed that SMF exposure did not exert any DNA damage in groups 1 and 2. However, it induced a low level of DNA single strand breaks in cells of group 3. To further explore the oxidative DNA damage, cellular DNA for group 3 was isolated, hydrolyzed and analysed by HPLC-EC. The level of 8-oxodGuo in this group remained unchanged compared to the sham exposed group (+6.5%, p > 0.05). Cells stained with zinc-specific fluorescent probes zinpyr-1 showed a decrease of labile zinc fraction in all groups exposed to SMF.Our data showed that SMF exposure (250 mT, during 3 h) did not cause oxidative stress and DNA damage in THP1 cells. However, SMF could alter the intracellular labile zinc fraction.

Effects of ageing on nuclear DNA integrity and metabolism in mussel cells (Mytilus edulis L.)

As the age of a cell increases, so does the potential for DNA damage. Recent theories on ageing suggest accumulative DNA damage is the primary cause of cellular senescence, possibly due to the decreased ability of DNA to act as a template for gene expression.In this paper we investigate the effects of ageing on the level of nuclear DNA damage in tissues of wild mussels of three different age groups; 2–4 years (group I), 6–8 years (group II) and 10 years (group III). In the digestive gland and haemolymph cells, a significant age-dependent increase of DNA damage was observed, as evaluated by the fluorimetric alkaline DNA unwinding technique, which is able to detect both direct single strand DNA breaks as well as alkali-labile apurinic sites.In addition, the rate of DNA polymerase activity was studied in order to determine whether DNA damage was dependent on DNA alteration, or because of a reduced rate of DNA repair. Unscheduled DNA repair synthesis in isolated nuclei of digestive gland cells in older mussels, was significantly decreased in comparison to younger mussels (−42% in group II and −37% in group III, p<0.01). In the digestive gland, salt extraction gives a slight, but significant, decrease of aphidicolin-sensitive DNA polymerase activity in age group III of −25%, p<0.05.Finally, we looked at the age variation in relation to oxidative stress. This was evaluated by measuring malondialdehyde accumulation in mussel cells. Digestive gland cells of group III, showed a significant age-related increase in malondialdehyde content of 170%, p<0.01, indicative of enhanced peroxidative processes.Taken together, these data suggest that the accumulation of DNA damage in group II is mainly dependent on the impairment of DNA repair systems. This is contrary to group III DNA damage, where a possible relationship between oxidative stress and alteration of nuclear DNA metabolism is found, probably deriving from an antioxidant defence decline.

DNA Damage in Diabetes: Correlation with a Clinical Marker

Levels of DNA damage in groups of 10 patients with insulin-dependent diabetes mellitus and 10 matched controls were compared using the comet assay; DNA strand breaks, oxidized pyrimidines (endonuclease III-sensitive sites) and altered purines (sites sensitive to formamidopyrimidine glycosylase) were measured. Mean values of strand breaks and oxidized pyrimidines were significantly higher in diabetics. Strand breaks correlated with body mass index in the diabetic group. A strong correlation was seen between formamidopyrimidine glycosylase-sensitive sites and serum glucose concentrations. When three patients with normal glucose levels were excluded from the statistical analysis, the mean value of formamidopyrimidine glycosylase-sensitive sites was very significantly elevated compared with normal. DNA damage in lymphocytes is thus a useful marker of oxidative stress, and in particular formamidopyrimidine glycosylase-sensitive sites seem to represent changes specifically related to hyperglycemia.