Taha A. Kumosani1,2,3, Elie Barbour2,3, Soonham S. Yaghmoor2,3, Said S. Moselhy4*
1Biochemistry Department, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia
2Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia
3Production of Bio-products for Industrial Application Research Group, King Abdulaziz University. Jeddah, Saudi Arabia
4Biochemistry Department, Faculty of Science, Ain Shams University, Cairo, Egypt
*Corresponding author’s email: moselhy6@hotmail.com
Received: 02 January 2026 / Revised: 10 February 2026 / Accepted: 19 February 2026 / Published Online: 08 March 2026
Abstract
Exposure to heavy metals such as nickel can affect many vital organs such as liver, kidney, and nervous system. The current study investigated the neurotoxicity of nickel sulfate in rats and the potential of histidine and its dipeptide derivative (carnosine) in abrogation of this toxicity. The present study was carried out on a total of 48 male Albino rats (100 ±10g). Rats were randomly equally grouped into six (8 rats each). Group I: Control. Group II: Rats received histidine chloride (10 mg/Kg b.w/day) orally for 30 days. Group III: Rats received carnosine (10 mg/Kg b.w/day) orally for 30 days. Group IV: Rats were injected i.p with (20 mg/kg b.w) daily of nickel sulfate for 30 days. Group V: Rats were injected i.p with 20 mg/kg daily of nickel sulfate and histidine chloride orally (10 mg/Kg b.w) for 30 days. Group VI: Rats were injected i.p with (20 mg/kg b.w) of nickel sulfate and carnosine orally (10 mg/Kg b.w) for 30 days. Data showed that nickel administration caused a significant decrease in hemoglobin and GSH levels, elevation of serum MDA, NO, IL-6, TNF-α levels, reduction in the activities of SOD and catalase. In addition, in brain tissue, a significant decrease in the levels of epinephrin, serotonin and ATP levels and acetylcholine esterase activity while increased in glycogen phosphorylase activity. The histidine or carnosine improved and recovered abnormalities induced by nickel significantly compared with untreated. The carnosine showed more effectiveness than histidine. In conclusion, the histidine or its derivative carnosine use is promising in preventing neurotoxicity induced by environmental pollution by nickel via anti-inflammatory, antioxidant and keep energy level of brain tissue.
Keywords: Carnosine, Histidine, Neurotoxicity, Nickel sulfate, Oxidative stress, Rats
