Methods: The scanning electron microscopy-energy dispersive X-ray spectroscopy (SEM-EDX) was used to qualitatively detect the cellular accumulation of ZnO NPs in algal cells, while inductively coupled plasma optical emission spectrometry (ICP OES) was performed to quantify the cell associated-zinc in algal cells. The percentage of cell death, reduction in algal biomass, and loss in photosynthetic pigments were measured to investigate the cytotoxic effects of ZnO NPs on H. pluvialis. Extracellular and intracellular changes in algal cells resulted from the treatment of ZnO NPs were demonstrated through optical, scanning, and transmission electron microscopic studies.
Results: SEM-EDX spectrum evidenced the accumulation of ZnO NPs in algal biomass and ICP OES results reported a significant (p < 0.05) dose- and time-dependent accumulation of zinc in algal cells from 24 h for all the tested concentrations of ZnO NPs (10-200 μg/mL). Further, the study showed a significant (p < 0.05) dose- and time-dependent growth inhibition of H. pluvialis from 72 h at 10-200 μg/mL of ZnO NPs. The morphological examinations revealed substantial surface and intracellular damages in algal cells due to the treatment of ZnO NPs.
Discussion: The present study reported the significant cellular accumulation of ZnO NPs in algal cells and the corresponding cytotoxic effects of ZnO NPs on H. pluvialis through the considerable reduction in algal cell viability, biomass, and photosynthetic pigments together with surface and intracellular damages.
METHODS: The cytotoxic effects were all assessed through quantification of loss in cell viability, reduction in biomass and decrease in photosynthetic pigments such as chlorophyll-a, carotenoids and phycocyanin. The surface interactions of nanoparticles and the subsequent morphological alterations on algal cells were examined by optical and scanning electron microscopy (SEM). The intracellular alterations of algal cells were studied using transmission electron microscopy. Furthermore, Fourier transformed infrared (FTIR) spectrum was obtained to investigate the involvement of algal surface biomolecules in surface binding of ZnO NPs on algal cells.
RESULTS: The treatment of ZnO NPs on S. platensis exhibited a typical concentration- and time-dependent cytotoxicity. Results showed a significant (p S. platensis triggered substantial cytotoxicity and caused cell death. Hence, S. platensis could be potentially used as a bioindicator for testing toxicity of ZnO NPs in aquatic environment.
METHODS: B. subtilis was exposed to 5 to 150 μg/mL of ZnO NPs for 24 h. The parameters employed to evaluate the antimicrobial potential of ZnO NPs were the growth inhibitory effect on B. subtilis, the surface interaction of ZnO NPs on the bacterial cell wall, and also the morphological alterations in B. subtilis induced by ZnO NPs.
RESULTS: The results demonstrated a significant (p <0.05) inhibition of ZnO NPs on B. subtilis growth and it was in a dose-dependent manner for all the tested concentrations of ZnO NPs from 5 to 150 μg/mL at 24 h. Fourier transformed infrared (FTIR) spectrum confirmed the involvement of polysaccharides and polypeptides of bacterial cell wall in surface binding of ZnO NPs on bacteria. The scanning electron microscopy (SEM) was used to visualize the morphological changes, B. subtilis illustrated several surface alterations such as distortion of cell membrane, roughening of cell surface, aggregation and bending of cells, as well as, the cell rupture upon interacting with ZnO NPs for 24 h.
CONCLUSION: The results indicated the potential of ZnO NPs to be used as an antibacterial agent against B. subtilis. The findings of the present study might bring insights to incorporate ZnO NPs as an antibacterial agent in the topical applications against the infections caused by B. subtilis.
METHODS: The interaction and accumulation of Ag NPs on A. platensis were examined through Fourier transformed infrared (FTIR) spectroscopy and scanning electron microscope (SEM). The loss in biomass together with the macromolecules, pigments, and phenolic compounds of A. platensis was investigated upon treating with various concentrations of Ag NPs (5, 10, 25, 50 and 100 µg/mL) for 24, 48, 72 and 96 h.
RESULTS: The results showed that the treatment of A. platensis with Ag NPs caused a dose and time-dependent reduction in biomass, macronutrients, pigments and phenolic compounds. The highest detrimental effects were found at 96 h with the reported values of 65.71 ± 2.79%, 67.21 ± 3.98%, 48.99 ± 4.39% and 59.62 ± 3.96% reduction in biomass, proteins, carbohydrates and lipids, respectively, along with 82.99 ± 7.81%, 67.55 ± 2.63%, 75.03 ± 1.55%, and 63.43 ± 2.89% loss in chlorophyll-a, carotenoids, C-phycocyanin, and total phenolic compounds of A. platensis for 100 µg/mL of Ag NPs. The EDX analysis confirmed the surface accumulation of Ag NPs on Arthrospira cells, while SEM images evidenced the surface alterations and damage of the treated cells. The functional groups such as hydroxyl, amine, methyl, amide I, amide II, carboxyl, carbonyl and phosphate groups from the cell wall of the A. platensis were identified to be possibly involved in the interaction of Ag NPs with A. platensis.
CONCLUSION: The study confirmed that the exposure of Ag NPs is detrimental to A. platensis where the interaction and accumulation of Ag NPs on A. platensis caused reduction in biomass, macromolecules, pigments, and total phenolic compounds.
OBJECTIVE: The aim of this study was to analyse epidemiological factors of periodontal disease among a south Indian population based on the role of sociodemographic factors, habitual factors and set of oral health knowledge, attitude, and behaviour measures.
METHODS: A sample of 288 participants above 18 years of age residing in Tamil Nadu, India took part in this cross-sectional study. Based on WHO criteria, periodontal disease was measured in our study. Age, ethnicity, smoking, education, and oral health behavior were found to be the covariates. Ordinal logistic regression analysis using R version 3.6.1 was utilized to study the various factors that influence periodontal disease among south Indian adults.
RESULTS: Various demographic factors such as age between 25 and 34 years (AOR = 2.25; 95% CI 1.14-4.55), 35-44 years (AOR = 1.80; 95% CI 0.89-3.64), ≥ 45 years old (AOR = 2.89; 95% CI 1.41-6.01), ethnicity (AOR = 2.71; 95% CI 1.25-5.81), smoking (AOR = 0.38; 95% CI 0.16-0.65), primary level education (AOR = 0.07; 95% CI 0.01-0.50) high school level education (AOR = 0.06; 95% CI 0.01-0.27), university level education (AOR = 0.08; 95% CI 0.01-0.36) and an individual's oral health behavior (AOR = 0.59; 95% CI 0.32-1.08) were found to be related with periodontal disease among the south Indian population. The maximum log likelihood residual deviance value was 645.94 in the final model.
CONCLUSION: Based on our epidemiological findings, sociodemographic, habitual factors and oral health behavior play a vital role in an individual's periodontal status among south Indian adults. An epidemiological model derived from the factors from our study will help to bring better understanding of the disease and to implement various preventive strategies to eliminate the causative factors.