99mTc-DMSA and 99mTc-DTPA identified renal dysfunction due to microplastic polyethylene in murine model
Javeria Zaheer, Joycie Shanmugiah, Seungyoun Kim, Hyeongi Kim, In Ok Ko, Byung Hyun Byun, Myeong A Cheong, Seung-Sook Lee, Jin Su Kim
Abstract
In the previous study (Im et al., 2022), we revealed microplastic (MP) was accumulated and cleared through the kidneys via PET imaging. Here, we aimed to identify the renal dysfunction due to polyethylene (PE) MP in the kidney tissue. Mice were exposed to 100 ppm (∼equivalent to 0.1 mg/mL)/100 μL of PE for 12 weeks (n = 10). PE uptake in the kidney tissues was confirmed using confocal microscopy. QuantSeq analysis was performed to determine gene expression. Renal function assessment was performed using 99m Tc-Diethylene triamine penta acetic acid or 99m Tc-Dimercaptosuccinic acid. Measurement of creatinine, BUN, and albumin levels in serum and urine samples was also estimated. [ 18 F]-FDG was also acquired. PE increased expression of Myc , CD44, Programmed Death-Ligand 1 (PD-L1), and Hypoxia-Inducible Factor (HIF)-1α, which indicates a potential link to an increased risk of early-onset cancer. An increase in glucose metabolism of [ 18 F]-FDG were observed. We assessed renal failure using 99m Tc-Diethylene triamine penta acetic acid and 99m Tc-Dimercaptosuccinic acid scintigraphy to determine the renal function. Renal failure was confirmed using serum and urine creatinine, serum blood urea nitrogen levels, serum albumin levels, and urine albumin levels in PE exposed mice, relative to the control. In sum, PE exposure induced renal dysfunction in a murine model. • 99m Tc-DMSA and 99m Tc-DTPA identified renal dysfunction induced by PE exposure. • Administration of PE to mice resulted in altered gene expression in the kidneys. • PE exposure increased the risk of renal cancer onset.