Effect of Carbamazepine, Ibuprofen, Triclosan and Sulfamethoxazole on Anaerobic Bioreactor Performance: Combining Cell Damage, Ecotoxicity and Chemical Information

Abstract

Pharmaceuticals and personal care products (PPCPs) are partially degraded in wastewater treatment plants (WWTPs), thereby leading to the formation of more toxic metabolites. Bacterial populations in bioreactors operated in WWTPs are sensitive to different toxics such as heavy metals and aromatic compounds, but there is still little information on the effect that pharmaceuticals exert on their metabolism, especially under anaerobic conditions. This work evaluated the effect of selected pharmaceuticals that remain in solution and attached to biosolids on the metabolism of anaerobic biomass. Batch reactors operated in parallel under the pressure of four individual and mixed PPCPs (carbamazepine, ibuprofen, triclosan and sulfametoxazole) allowed us to obtain relevant information on anaerobic digestion performance, toxicological effects and alterations to key enzymes involved in the biodegradation process. Cell viability was quantitatively evaluated using an automatic analysis of confocal microscopy images, and showed that triclosan and mixed pollutants caused higher toxicity and cell death than the other individual compounds. Both individual pollutants and their mixture had a considerable impact on the anaerobic digestion process, favoring carbon dioxide production, lowering organic matter removal and methane production, which also produced microbial stress and irreversible cell damage.

Advances in Antioxidant Applications for Combating 131I Side Effects in Thyroid Cancer Treatment

“…Comparatively, a GSH deficiency disrupts the REDOX homeostasis, causing ROS accumulation, which eventually results in cell death. The CAT and SOD enzymes play a key role in free radical management, and their reduced activity contributes to an increase in the accumulation of O 2− and H 2 O 2 [ 65 , 66 , 67 , 68 , 69 , 70 , 71 ]. Additionally, excessive ROS interact with specific cellular targets to trigger a cascade reaction involving polyunsaturated fatty acid free radicals (lipid peroxidation) on the cell membranes, resulting in an increase in the malondialdehyde (MDA) (marker of lipid peroxidation) levels and a decrease in the CAT, SOD, and GSH activity, resulting in an imbalance between oxidants and antioxidants.…”

“…Comparatively, a GSH deficiency disrupts the REDOX homeostasis, causing ROS accumulation, which eventually results in cell death. The CAT and SOD enzymes play a key role in free radical management, and their reduced activity contributes to an increase in the accumulation of O 2− and H2O2 [65][66][67][68][69][70][71]. Additionally, excessive ROS interact with specific cellular targets to trigger a cascade reaction involving polyunsaturated fatty acid free radicals (lipid peroxidation) In contrast, although most radiation from RAI enters the thyroid gland, a small amount of 131 I present in the blood and tissues is also capable of causing radiation in other parts of the body [75], such as lipid peroxidation in the kidney, salivary glands, and erythrocytes, resulting in structural and functional damage to the cells [22,75].…”