World Journal of Pharmacology and Toxicology
Open Access

Neurotoxicology; Endocrine disruption; Hormonal signaling pathways; Environmental exposures; Environmental neurotoxicants

Introduction

The intricate relationship between neurotoxicology and endocrine disruption has emerged as a compelling area of research, drawing attention to the interconnectedness of the nervous and endocrine systems and the potential synergistic impact of environmental exposures. Neurotoxicology investigates the adverse effects of substances on the nervous system, encompassing a spectrum of compounds capable of influencing neural structure and function. Concurrently, endocrine disruption focuses on the perturbation of the endocrine system, particularly the intricate network of hormones that regulate various physiological processes. The Central Nervous System (CNS) and the endocrine system are not isolated entities; rather, they share a dynamic interplay crucial for maintaining homeostasis and orchestrating fundamental developmental processes. Hormones, key mediators in the endocrine system, exert profound influences on neurodevelopment, synaptic plasticity, and neurotransmission. Disruptions to this delicate balance, whether through exposure to neurotoxicants or Endocrine-Disrupting Chemicals (EDCs), have the potential to induce adverse effects that extend across both systems [1,2].

Discussion

Neurotoxicology and endocrine disruption are two distinct fields of study, but there is growing recognition that they can be interconnected. Both neurotoxicology and endocrine disruption involve the impact of certain substances on biological systems, but they focus on different aspects of the body.

Neurotoxicology

Neurotoxicology is the study of substances that have the potential to harm the nervous system. These substances, known as neurotoxins, can affect the structure or function of the nervous system, leading to various adverse effects on behavior, cognition, and other neurological functions. Neurotoxic substances can include heavy metals, pesticides, certain drugs, and industrial chemicals. The impact of neurotoxic substances can be acute or chronic, depending on factors such as dose, duration of exposure, and individual susceptibility. The nervous system is highly sensitive to chemical insults, and exposure to neurotoxic substances can result in neurodevelopmental disorders, neurodegenerative diseases, and other neurological conditions [3,4].

Endocrine disruption

Endocrine disruption refers to the interference with the endocrine system, which is responsible for regulating hormone production and signaling. Endocrine Disrupting Chemicals (EDCs) can mimic or interfere with the body's hormones, leading to disruptions in normal physiological functions. EDCs can include substances such as phthalates, Bisphenol A (BPA), pesticides, and certain pharmaceuticals [6,7]. These chemicals may affect the endocrine system by binding to hormone receptors, altering hormone production, or interfering with hormone signaling pathways. Endocrine disruption has been associated with a range of health effects, including reproductive disorders, developmental abnormalities, and an increased risk of certain cancers [8].

The connection between neurotoxicology and endocrine disruption arises because the nervous system and the endocrine system are intricately linked [9]. Hormones produced by the endocrine system play crucial roles in the development and function of the nervous system. Disruptions in hormone signaling can have cascading effects on neurological processes. For example, exposure to certain EDCs during critical periods of neurodevelopment may lead to alterations in brain structure and function. Additionally, some neurotoxic substances may exert their effects through interactions with the endocrine system [10].

Conclusion

In conclusion, this review underscores the importance of integrating neurotoxicology and endocrine disruption research, providing a foundation for future investigations into the complex interactions between environmental exposures and human health. Such an integrated approach is essential for advancing our understanding of the mechanisms underlying neuroendocrine disruptions and for informing strategies to safeguard vulnerable populations from the adverse consequences of combined exposures.

1. Lurlaro R, Muñoz Pinedo C (2016) Cell death induced by endoplasmic reticulum stress. FEBS J. 283: 2640-2652.

Indexed at, Google Scholar, Crossref

2. Braakman I, Hebert DN (2013) Protein folding in the endoplasmic reticulum. Cold Spring Harb Perspect. Biol. 5: a013201.

Indexed at, Google Scholar, Crossref

3. Luo B, Lee AS (2013) The critical roles of endoplasmic reticulum chaperones and unfolded protein response in tumorigenesis and anticancer therapies. Oncogene. 32: 805-818.

Indexed at, Google Scholar, Crossref

4. Lukas J, Pospech J, Oppermann C, Hund C, Iwanov K et al. (2019) Role of endoplasmic reticulum stress and protein misfolding in disorders of the liver and pancreas. Adv Med Sci. 64: 315-323.

Indexed at, Google Scholar, Crossref

5. Cao SS, Kaufman RJ (2014) Endoplasmic reticulum stress and oxidative stress in cell fate decision and human disease. Antioxid. Redox Signal. 21: 396-413.

Indexed at, Google Scholar, Crossref

6. Houck SA, Ren HY, Madden VJ, Bonner JN, Conlin MP et al. (2014) Quality control autophagy degrades soluble ERAD-resistant conformers of the misfolded membrane protein GnRHR. Mol Cell. 54: 166-179.

Indexed at, Google Scholar, Crossref

7. Gessner DK, Schlegel G, Ringseis R, Schwarz FJ, Eder K (2014) Up-regulation of endoplasmic reticulum stress induced genes of the unfolded protein response in the liver of periparturient dairy cows. BMC Vet. Res. 10: 46.

Indexed at, Google Scholar, Crossref

8. Malhotra JD, Kaufman RJ (2007) Endoplasmic reticulum stress and oxidative stress: A vicious cycle or a double-edged sword? Antioxid Redox Signal. 9: 2277-2293.

Indexed at, Google Scholar, Crossref

9. Tse G, Yan BP, Chan YW, Tian XY, Huang Y (2016) Reactive oxygen species, endoplasmic reticulum stress and mitochondrial dysfunction: The link with cardiac arrhythmogenesis. Front Physiol. 7: 313.

Indexed at, Google Scholar, Crossref

10. Hotamisligil GS (2010) Endoplasmic reticulum stress and the inflammatory basis of metabolic disease. Cell. 140: 900-917.

Indexed at, Google Scholar, Crossref