L-Theanine Protects Against Bisphenol A-Induced Neurodegeneration and Cognitive Deficits

Abstract

Objective: Bisphenol A (BPA), an endocrine-disrupting compound, increases the production of reactive oxygen species, leading to mitochondrial dysfunction and oxidative damage. This study aimed to assess the neuroprotective effects of L-theanine (LTN), an amino acid found in tea leaves, against BPA induced oxidative neurodegeneration and cognitive dysfunction in rats.Materials and Methods: Animals were allocated into four experimental groups, each containing eight rats: Control, LTN, BPA, and BPA+LTN groups. BPA was administered via drinking water at a concentration adjusted to achieve an estimated daily intake of approximately 50 mg/kg for 4 weeks, whereas L-theanine (LTN, 100 mg/kg/day) was administered orally by gavage. Cognitive function tests were conducted at the end of the treatment period, and the rats were then decapitated to collect brain tissue samples for biochemical analyses, including acetylcholinesterase (AChE) and caspase-3 protein levels, as well as levels of amyloid beta, glutathione (GSH), lipid peroxidation (LPO), and 8-hydroxy-2'-deoxyguanosine (8-OHdG).Results: Cognitive tests, Morris water maze, and novel object recognition tests showed that BPA-induced cognitive deficits improved in the LTN group. Furthermore, BPA caused significant increases in AChE and caspase-3 protein levels, as well as in amyloid beta, LPO, and 8-OHdG levels, whereas GSH, a key antioxidant, was decreased. LTN reversed these alterations, restoring them to values in the control group.Conclusion: BPA caused neuronal oxidative damage and cognitive dysfunction in rats, and LTN treatment significantly attenuated these alterations via neuroprotective mechanisms.