The novel role of the aquaporin water channel in lycopene preventing DEHP-induced renal ionic homeostasis disturbance in mice

Di-(2-ethylhexyl) phthalate (DEHP), an extensively used plasticizer, can cause environmental pollution and organ injury. Lycopene (LYC) is a natural carotene that has the potential to prevent chronic diseases. To reveal the effect of DEHP and/or LYC on the kidney, male mice were treated with LYC (5 mg/kg) and/or DEHP (500 mg/kg or 1000 mg/kg) by gavage for 28 days. The study indicated that DEHP caused glomerular atrophy, tubular expansion, disappearance of the mitochondrial membrane, and cristae rupture. DEHP exposure can increase the expression of aquaporin (AQP) subunits and the activity of Ca2+-Mg2+-ATPase and decrease the activity of Na+-K+-ATPase, which results in ion disorder. However, LYC can relieve kidney injury by regulating the activity of ATPase, the expression of ATPase subunits, and AQP subunit expression. The results indicated that AQP was a target for LYC in antagonizing the disturbance of DEHP-induced renal damage. The present results indicated that AQP was a target for LYC to antagonize the disturbance of DEHP-induced renal ion homeostasis and renal injury. This research might provide a feasible molecular mechanism for LYC cotreatment of renal toxicity caused by DEHP. [Display omitted] •DEHP exposure induced nephrotoxicity.•DEHP can cause the ions homeostasis imbalance.•DEHP caused the expression of AQP and ATPase activity disorder.•LYC can protect the organism from DEHP-induced nephrotoxicity.