TNF-α detection using gold nanoparticles as a surface-enhanced Raman spectroscopy substrate.

Background: TNF-α is a cytokine involved in inflammation. Surface-enhanced Raman spectroscopy (SERS) could be useful in its detection. Aim: Identify the TNF-α in an aqueous solution, using gold nanoparticles (AuNPs) as a SERS substrate. Materials & methods: Raman and SERS spectra were obtained from TNF-α samples, combined with AuNPs, with decreasing concentrations of TNF-α. The samples were analyzed using optical transmission spectroscopy, dynamic light scattering, and transmission electron microscopy. Results: Transmission electron microscopy/dynamic light scattering determined a change in the average diameter of the TNF-α/AuNPs (∼9.6 nm). Raman bands obtained were associated with aromatic amino acid side chains. We observe Raman signals for TNF-α concentrations as low as 0.125 pg/ml. Conclusion: TNF-α signal at physiological concentrations was determined with SERS.

Exposure to arsenic and lead in children from Salamanca México, effects on telomeric lengthening and mitochondrial DNA.

Levels of urinary arsenic and levels of lead in blood were measured in children attending elementary schools located in an industrial zone in Salamanca, México. Its possible effects using telomere length and mitochondrial DNA copy number as biomarkers of genomic disequilibrium by oxidative stress were studied. Eighty-eight children (6-15 years old) were included and urine samples were collected for quantification of arsenic, while lead was measured in blood samples using inductively coupled plasma mass spectrometry (ICP-MS). DNA was isolated from peripheral blood and relative telomere length and the mitochondrial DNA copy number were determined by real-time PCR. The geometric mean of urinary arsenic was 54.16 µg/L (11.7-141.1 µg/L). Ninety-eight percent of the children were above 15 µg/L (biomonitoring equivalent value). With respect to the concentration of lead in blood, the mean was 3.78 µg/dL (LOD-22.61), where 24.5% of the participants had equal or above the reference value (5 µg/dL; Mexican Official Norm NOM-199-SSA1-2000, 2017). A positive association between urinary arsenic and telomere length was found (ß = 0.161; 95% CI: 0.12; 0.301; P = 0.034), while lead blood concentrations were negatively associated with mitochondrial DNA copy number (ß = - 0.198; 95% CI: - 2.81; - 0.17; P = 0.019), after adjusting by age, sex, and total white blood cell count. Differences in the mitochondrial DNA content were observed in children with lead blood levels from 2.5 µg/dL, (P ≤ 0.001), suggesting an effect at lead exposure levels considered acceptable (< 5 µg/dL). In conclusion, children living in an industrial area in Salamanca showed an exposure to arsenic and lead and an impact on telomere length and mitochondrial DNA content associated with arsenic and lead exposure, respectively.

Association of Leukocyte Telomere Length and Mitochondrial DNA Copy Number in Children from Salamanca, Mexico.

AIM: The purpose of this study was to determine if there is a correlation between telomere length (TL) and mitochondrial DNA copy number (mtDNAcn) in children. METHODS: Leukocyte TL and mtDNAcn were measured by real-time PCR in 98 Mexican children 6-12 years of age from Salamanca, México. RESULTS: A positive association was found between TL and mtDNAcn after a natural log transformation (Pearson correlation r = 0.72; p < 0.0001). No correlation between age and body mass index (BMI) biomarkers was found, and no differences according to sex were observed. After adjustment for these variables, a linear regression model showed an association between TL and mtDNAcn (ß = 0.739, 95% confidence interval 0.594; 0.885, p < 0.0001). CONCLUSIONS: A strong positive correlation between TL and mtDNAcn was found in the study population; age, sex, and BMI seemed to have no effect on this correlation.