Zinc and L-carnosine are biologically active agents of increasing clinical importance in psychiatry. Zinc is essential for enzymatic catalysis, maintenance of protein structural integrity, regulation of cellular signaling, neurotransmission, synaptic plasticity, neurogenesis, and antioxidant defense. Disturbances in zinc homeostasis are associated with depression, schizophrenia, attention deficit/hyperactivity disorder, and Alzheimer’s disease. Meanwhile, L-carnosine, a dipeptide abundant in the nervous tissue, has antioxidant, anti-inflammatory, anti-glutamatergic, histamine-enhancing, metal-chelating, and neuroprotective properties. It also enhances zinc bioavailability by promoting intestinal absorption and acting as a zinc ionophore to facilitate cellular uptake. The zinc–L-carnosine complex (polaprezinc) is a drug used to treat gastric ulcers. This combination provides mechanistic benefits that extend beyond gastrointestinal indications, offering synergistic and multifaceted effects. It mitigates oxidative stress and neuroinflammation, modulates the transmission of glutamate, γ-aminobutyric acid, and serotonin, enhances histamine production, and increases neurotrophic factor levels. It may also regulate synaptic zinc homeostasis and protect neurons from excess zinc-induced neurotoxicity. Emerging clinical evidence suggests that zinc–L-carnosine combination therapy can treat various psychiatric disorders plausibly related to zinc deficiency, including binge eating disorder, bulimia nervosa, dissociative identity disorder, and burning mouth syndrome. Symptoms such as flashbacks, self-harm, and hypersomnia may also respond to treatment. This review summarizes the molecular mechanisms and clinical findings for zinc, L-carnosine, and their combinations in the treatment of psychiatric conditions. While the current evidence is preliminary, the natural origin, favorable safety profile, and clinical feasibility of this combination therapy support further controlled investigations as an integrative nutritional-neuropsychiatric strategy for these difficult-to-treat conditions.

The kidney is the primary site of uranium (U) deposition after exposure. The distal portion—S3 segment of the proximal tubules may be involved in U reabsorption from the urine. However, the dynamics of the U distribution in renal tubules have not yet been clearly understood. This study precisely examined the distribution of U within the S3 segment (S3 tubules) in male Wistar rats during the initial phase (1–3 h) of subcutaneous administration with uranyl acetate (UA), 0.5 mg/kg of body weight. X-ray fluorescence spectrometry with a high-energy synchrotron radiation microbeam (SR-μXRF) was employed. At 1 h of administration, U was rapidly transported into the kidneys and accumulated at 4% of the dose. A cross-section of the S3 tubules revealed a distribution of U within the brush border, indicating that U reabsorption was in-progress at this time point. Enhanced U accumulation with a maximum of 134 μg/g was also detected in the epithelium of the S3 tubule microregions. At 3 h, U accumulation in the kidneys was 9%, and U microlocalization in the S3 tubule epithelium reached approximately 200 μg/g. These microlocalization distribution patterns were characteristic of U and differed from those of endogenous trace elements, such as iron and zinc. These findings are valuable for designing decorporation strategies applicable to the U accumulated in this critical organ.