Abstract

Neurotoxicity-injury to the nervous system resulting from chemical, biological, or physical insults-remains a 
pressing clinical and public-health problem across acute exposures (organophosphates, heavy metals, 
chemotherapeutics), chronic environmental pollution, and neurodegenerative disorders where toxic processes 
(oxidative stress, mitochondrial dysfunction, excitotoxicity, neuroinflammation) play central roles. Antioxidant 
herbal remedies, composed of polyphenols, flavonoids, alkaloids and other phytochemicals, are widely proposed as 
neuroprotective agents because they modulate redox balance, mitochondrial function, and inflammatory signaling. 
Preclinical literature overwhelmingly supports multi-modal neuroprotection for compounds such as curcumin, 
resveratrol, quercetin, epigallocatechin gallate (EGCG), ginsenosides and berberine across models of ischemia, 
toxin-induced neuronal death, and protein-aggregation pathology. However, clinical translation is limited: human 
trials are small, heterogeneous in formulations and outcomes, and frequently confounded by poor bioavailability and 
inadequate safety monitoring. Furthermore, some herbal extracts carry intrinsic neurotoxic or pro-oxidant risks at 
high doses or via contaminants and interactions. This review synthesizes mechanistic rationales for antioxidant 
phytotherapy in neurotoxicity, critically examines preclinical and clinical evidence, highlights safety and 
standardization challenges, and proposes research priorities standardized extracts, rigorous pharmacokinetics, 
mechanistic biomarkers, and well-powered randomized trials to clarify whether antioxidant herbal remedies can be 
responsibly integrated into neuroprotective strategies. Until such evidence is available, herbal antioxidants should 
be considered experimental adjuncts rather than established neurotherapeutics.