Recreational ketamine exposure disrupts redox and inflammatory homeostasis in salivary glands and plasma leading to salivary dysfunction.

Abstract

Recreational ketamine use has become an increasing public health concern due to its systemic toxic effects; however, its impact on salivary gland homeostasis and salivary function remains poorly understood, particularly regarding the oxidative and inflammatory mechanisms involved. Therefore, this study investigated the effects of repeated ketamine exposure on plasma, saliva, and major salivary glands through the assessment of oxidative stress biomarkers, inflammatory mediators, and salivary alterations in an experimental model. Ninety-day-old Wistar rats (Rattus norvegicus) were allocated into three groups: a control group receiving saline solution and ketamine-exposed groups treated with 25 mg/kg ketamine via intraperitoneal injection three times weekly for 2 or 4 weeks. At the end of the experimental periods, plasma, saliva, parotid, and submandibular glands were collected for biochemical analyses. Ketamine exposure significantly reduced antioxidant defenses, including glutathione levels and total antioxidant capacity, in plasma, saliva, and salivary glands. In parallel, lipid peroxidation and nitric oxide levels progressively increased, indicating marked redox imbalance. Ketamine administration also promoted a pronounced pro-inflammatory response characterized by increased IL-6, IL-8, TNF-α, and IFN-γ levels, accompanied by reduced IL-10 concentrations, particularly after 4 weeks of exposure. Regarding salivary function, ketamine exposure induced significant alterations in salivary composition, including increased amylase and mucin levels, associated with fluctuations in total protein concentrations, suggesting progressive secretory dysregulation and salivary gland dysfunction. Overall, repeated recreational ketamine exposure disrupts systemic and salivary gland redox-inflammatory homeostasis, leading to salivary dysfunction and reinforcing saliva and salivary glands as previously neglected targets of ketamine-induced toxicity.

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