Phycotoxicity of antibiotics and non-steroidal anti-inflammatory drugs to green algae Chlorella sp. and Desmodesmus spinosus: Assessment of combined toxicity by Box–Behnken experimental design
There is a growing concern regarding the adverse effects of pharmaceutical pollution on aquatic environments. The present study investigated the toxicity of different antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) on two green algae namely Chlorella sp. and Desmodesmus spinosus. Based on the 96h IC50 values of the two chlorophytes, tetracycline (TET) was more toxic than other antibiotics (ciprofloxacin (CPF) and amoxicillin (AMX)), while paracetamol (PAR) was more toxic than ketoprofen (KET) and diclofenac (DIF). Gross photosynthesis was markedly reduced with most of the investigated drugs, although, the Chl a content was stimulated in a dose-dependent manner. Algal treated cells exhibited elevated malonaldehyde content which reflected several structural and functional cellular damages. Catalase and ascorbate peroxidase (APX) were involved in the reduction of reactive oxygen species, but the effects of APX were more pronounced at low drug concentrations. Box–Behnken design (BBD) was employed to investigate the combined toxicities of PAR, KET, AMX and TET on D. spinosus in response to growth inhibition and pigment increase. The mutual interactions varied between synergism and antagonism. The BBD analysis indicated that the experimental design could be effectively utilized as a useful tool for ecotoxicological assessment.
contents with an increase in GSH content and SOD activity. Mechanistically, DADS effectively down-regulated mRNA expression level of renal p38 and NF-κB. Additionally, DADS positively regulated the NRF2 gene with a remarkable inhibition of Keap-1 gene. Furthermore, DADS up-regulated BCL2 protein and remarkably suppressed the expression of both BAX and caspase-3 proteins. Overall, DADS has favorable renal protection against MTX-induced nephropathy via modulation of Keap-1/NRF2, p38/NF-κB, and BCL2/BAX/caspase-3 signaling.