Study the effect of common contaminants on rat pancreatic cell physiology

Abstract

The neonicotinoid insecticide acetamiprid has been linked to toxicity in various organs and organisms. However, its effects on the exocrine pancreas remain largely unexplored. This study aimed to investigate the toxic effects of acetamiprid on the exocrine pancreas through in-vivo and in-vitro investigations. We also explored the potential preventive effects of carnosine. In the in-vivo study, male Wistar rats were administered acetamiprid orally at two doses (21.7 and 43.4 mg/kg/day, respectively) with or without carnosine supplementation (200mg/kg/day) for 30 days. The body and pancreatic weight were measured, malonaldehyde, glucose, lipase, amylase levels, and histopathological examination were evaluated. In the in-vitro study, AR42J pancreatic cells were exposed to acetamiprid with or without carnosine, and the cell viability, MAPK signaling pathway, intracellular calcium levels, and trypsin secretion were investigated. Sub-acute acetamiprid exposure led to significant adverse effects, including decreased body weight and pancreatic somatic index, increased blood glucose, altered pancreatic enzyme levels (decreased amylase and increased lipase levels), and elevated malondialdehyde levels. Histological examination revealed damage to pancreatic tissue. While carnosine supplementation partially mitigated these adverse effects. Acetamiprid exposure altered AR42J pancreatic cell viability in a dose-dependent manner, while co-treatment with carnosine significantly improved cell survival, and activated the MAPK signaling pathway, which was attenuated by carnosine. While acetamiprid increased intracellular calcium levels, it did not significantly affect trypsin secretion. This study shows that acetamiprid harms the exocrine pancreas. However, carnosine supplementation may offer protection against these harmful effects.