Antioxidant Potential of Lactoferrin and Its Protective Effect on Health: An Overview Original paper

What Was Reviewed?

The paper is a comprehensive review that consolidates current scientific understanding of lactoferrin (Lf) as a multifunctional protein with potent antioxidant and immune-regulating capabilities. The review explores lactoferrin’s capacity to modulate oxidative stress, regulate iron metabolism, and exert neuroprotective effects. Additionally, it highlights Lf’s therapeutic potential in chronic diseases such as cardiovascular disease, neurodegeneration (particularly Parkinson’s and Alzheimer’s), obesity, hepatitis, respiratory conditions, dry eye disease, anemia, and inflammation-driven conditions. The authors synthesize both in vitro and in vivo findings that underline the systemic effects of Lf across multiple organ systems, with a focus on its antioxidant, anti-inflammatory, and antimicrobial mechanisms.

Who Was Reviewed?

This review draws on a wide body of experimental and clinical studies involving animal models (e.g., Wistar rats, murine models of cystic fibrosis, and neonatal rat models of brain injury), human subjects (e.g., obese pediatric patients, pregnant women, athletes, individuals with anemia, and patients with neurodegenerative and liver diseases), and in vitro studies on human cell cultures. The subjects span age, species, and physiological status, enabling a multifaceted perspective on lactoferrin’s biological activities and clinical applicability.

What Were the Most Important Findings?

The review underscores that lactoferrin functions as a potent natural antioxidant, capable of neutralizing reactive oxygen species (ROS) and mitigating lipid peroxidation. It stimulates endogenous antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), often via Nrf2-dependent pathways. Lactoferrin’s iron-chelating activity plays a central role in minimizing iron-induced oxidative damage, particularly in neurodegenerative diseases. It regulates ferroptosis by altering the expression of iron transport and storage proteins, which is contextually beneficial—for instance, reducing ferroptosis in liver injury while promoting it in cancer therapy.

From a microbiome perspective, lactoferrin’s iron sequestration impairs biofilm formation in E. coli and other pathogens, suggesting prebiotic and antimicrobial benefits in the gastrointestinal tract. Furthermore, it interacts with receptors such as TLR4, CD14, CXCR4, and LRP1, mediating immune signaling and potentially influencing the composition and activity of microbial communities. The review also touches on how lactoferrin supports mucosal immunity and modulates cytokine expression, contributing to a stable and functional microbiome-host interface.

What Are the Implications of This Review?

Clinically, this review identifies lactoferrin as a promising therapeutic agent for preventing and managing chronic conditions characterized by oxidative stress, iron dysregulation, and immune imbalance. Its ability to modulate ROS, chelate iron, and activate host defense mechanisms without promoting microbial resistance or systemic toxicity offers a valuable alternative to conventional interventions. Its potential neuroprotective effects, particularly in Alzheimer’s and Parkinson’s diseases—may open pathways for non-invasive therapeutic strategies targeting the blood-brain barrier. Moreover, lactoferrin’s systemic influence on inflammation and microbial dynamics highlights its emerging role in microbiome-informed clinical practice. For clinicians, the evidence supports considering lactoferrin as a supplemental strategy in managing oxidative stress-related pathologies and enhancing gut-immune-brain axis resilience.