Phospholipids modifications, genotoxic and anticholinesterase effects of pepper fruit (Dennettia tripetala G. Baker) extract in Swiss mice.

The toxicity of D. tripetala fruit extract to mice was investigated using data obtained from lipidomic analyses, comet and Acetylcholinesterase (AChE) assays. Mice (n = 8) were exposed for 30 days via oral gavage to vehicle (5% Tween 80) (negative control), D. tripetala extract (100, 200 and 400 mg/kg) and 40 mg/kg methyl methanesulfonate (MMS) (positive control). The profile of compounds in the fruit extract was analyzed using gas chromatography-mass spectrometry. Out of the total of 32 compounds identified, considerable amount of established insecticidal compounds such as 2-phenylnitroethane, cis-vaccenic acid, linalool and linoleic acid were detected. Fruit extract did not induce DNA damage relative to negative control. Percentage gain in body weights differed significantly across the four weeks. Significantly highest and lowest brain AChE activity was observed in animals exposed to 200 and 400 mg/kg D. tripetala, respectively. Fruit extract modulated the brain phospholipid profile due to significant fold changes of 48 lipid species out of the total of 280 lipid species. High number of differentially expressed phosphatidylcholine (PC) species and significant levels of phosphatidylethanolamine (PE) at 400 mg/kg suggests that activation of inflammation and methylation pathways are the most plausible mechanisms of D. tripetala toxicity to mouse brain tissue.

DNA damage is inversely associated to blood levels of DHA and EPA fatty acids in Brazilian children and adolescents.

This study aimed to investigate the association between DNA damage and blood levels of docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), retinol, beta-carotene and riboflavin in Brazilian children and adolescents. Subjects (n = 140) were healthy boys and girls aged 9 to 13 years in Ribeirão Preto (SP, Brazil). Data collection included anthropometry, assessment of energy intake and blood sampling. DNA damage was evaluated by single-cell gel electrophoresis (comet assay). Principal component analysis (PCA) was used to verify associations between blood concentrations of vitamins, polyunsaturated fatty acids and DNA damage. Multiple regression analyses, k-means cluster, and analysis of covariance (ANCOVA), adjusted for confounding variables such as age, sex, energy intake, body mass index and total cholesterol (when needed), were applied to confirm the associations. PCA explained 69.4% of the inverse relationships between DNA damage and blood levels of DHA, EPA, retinol, and beta-carotene. Results were confirmed by ANCOVA and multiple regression analyses for DHA and EPA. In conclusion, omega-3-fatty acids were inversely associated with DNA damage in Brazilian children and adolescents and may be a protective factor against the development of future diseases.

Lead (Pb) exposure induces disturbances in epigenetic status in workers exposed to this metal.

Previous studies showed that lead (Pb) exposure may modulate gene expression by changes in the epigenetic status. However, little is known about the impact of Pb exposure and alterations on DNA methylation patterns in humans exposed to this metal. The aim of this study was to assess the consequences of exposure to Pb on DNA global methylation, in order to gain a better understanding of the interactions between Pb exposure and epigenetic effects. The study included 100 male workers employed in automotive battery factories from Paraná State, Brazil. Concentrations of Pb in blood (B-Pb) and plasma (P-Pb) were determined by ICP-MS, the percentage (%) of global DNA methylation was determined by quantification of 5-methylcytosine using indirect ELISA, and sociodemographic data collected by questionnaire by trained interviewers. The mean age was 37 ± 10 (18-67 years); 18% of participants were smokers, while 32% reported consumption of alcoholic beverages. The B-Pb and P-Pb levels were 20 ± 11 and 0.56 ± 0.64 µg/dl, respectively; % global DNA methylation was 2.8 ± 1.1% (ranging from 1.1 to 6.5%). B-Pb and P-Pb concentrations were significantly correlated. Furthermore, a marked association was noted between Pb biomarkers and DNA global methylation. Taken together, our data demonstrated that Pb exposure induced alterations on DNA global methylation in workers who were exposed to the metal and consequently may result in disturbances in the regulation of gene expression, leading to potentially several health adverse effect outcomes.

Effects of maternal vitamin B6 deficiency and over-supplementation on DNA damage and oxidative stress in rat dams and their offspring.

Vitamin B6 is a cofactor for more than 140 essential enzymes and plays an important role in maternal health and fetal development. The goal of this study was to investigate the effects of maternal vitamin B6 on DNA damage and oxidative stress status in rat dams and their offspring. Female Wistar rats were randomly assigned to three dietary groups fed a standard diet (control diet), a diet supplemented with 30 mg/kg of vitamin B6, or a deficient diet (0 mg/kg of vitamin B6) for 10 weeks before and during mating, pregnancy and lactation. The dams were euthanized at weaning, and their male pups were euthanized either 10 days or 100 days after birth. We found that maternal vitamin B6 deficiency increased the micronucleus frequency in peripheral blood and bone marrow cells and also increased the concentration of hepatic TBARS (thiobarbituric acid reactive substances) in newborn pups (10 days old). In conclusion, maternal 5- to 6-fold over-supplementation of vitamin B6 had no adverse effects, however its deficiency may induce chromosomal damage and hepatic lipid peroxidation in the offspring.