Medical Hypotheses
Volume 74, Issue 4 , Pages 698-701, April 2010

Luteinizing hormone provides a causal mechanism for mercury associated disease

  • Dan R. Laks

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    • Corresponding Author InformationTel.: +1 310 740 1483; fax: +1 310 206 5061.

Mental Retardation Research Center, David Geffen School of Medicine at UCLA, 635 Charles E. Young Dr. South, Neuroscience Research Building, Room 379 (lab), Los Angeles, CA 90095-7332, USA

Received 15 October 2009; accepted 18 October 2009. published online 16 November 2009.

Summary 

Previous studies have demonstrated that the pituitary is a main target for inorganic mercury (I-Hg) deposition and accumulation within the brain. My recent study of the US population (1999–2006) has uncovered a significant, inverse relationship between chronic mercury exposure and levels of luteinizing hormone (LH). This association with LH signifies more than its presumed role as bioindicator for pituitary neurosecretion and function. LH is the only hormone with a rare and well characterized, high affinity binding site for mercury. On its catalytic beta subunit, LH has the structure to preferentially bind inorganic mercury almost irreversibly, and, by that manner, accumulate the neurotoxic element. Thus, it is likely that LH is an early and significant target of chronic mercury exposure. Moreover, due to the role of LH in immune-modulation and neurogenesis, I present LH as a central candidate to elucidate a causal mechanism for chronic mercury exposure and associated disease.

Abbreviations: LH, luteinizing hormone, I-Hg, inorganic mercury, CH3Hg, methyl mercury, NHANES, national health and nutrition examination survey, AD, Alzheimer’s disease, HPA, hypothalamic–pituitary–adrenal axis

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PII: S0306-9877(09)00715-4

doi:10.1016/j.mehy.2009.10.036

Medical Hypotheses
Volume 74, Issue 4 , Pages 698-701, April 2010