Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers
 
 

 

 

Johansson, M, S Nilsson and BO Lund. 1998. Interactions between Methylsulfonyl PCBs and the Glucocorticoid Receptor. Environmental Health Perspectives. 106(12):769-777.


In this paper Johansson et al., are exploring why populations of gray seals and harbor seals in the Baltic Sea are suffering from claw deformities, adrenocortical hyperplasia and uterine lesions suspected to be the result of disruption of glucocorticoid homeostasis. They find that two common PCB metabolites interact with the glucocorticoid receptor, but that a third PCB metabolite does not.

In humans, excessive production of glucocorticoids can result in obesity, protein wasting, immunosuppression, insulin resistence (that can lead to diabetes), osteoporosis, growth retardation and hypertension. A deficiency of glucocorticoids can result in gastrointestinal problems, weight loss, mental confusion, hypoglycemia, hypotension and increased insulin sensitivity.

In their experiments they examined competition for binding with the glucocorticoid receptor between the PCBs and dexamethasone, a drug known to act as a competitive antagonist for the glucocorticoid receptor. The two active metabolites were MeSO2-CB149 and 3-MeSO2-CB101, both methylsulphone PCBs. MeSO2-CB149 competed for binding with dexamethasone with an affinity 10 times lower than 3- MeSO2-CB149.

Johansson et al. also note that although these methylsulphonyl PCBs are two of the most abundant pollutants in Sweden and Canadian biota, little research has been done to examine their biological effects.

This study is significant for two reasons:

  • It demonstrates the ability of environmental chemicals to interfere with yet another hormone system, the human cortisol signalling system, via interference with the glucocorticoid receptor.
  • The study examines three methysulphonyl PCB metabolites and reports different binding affinities in two and no binding affinity in the third. This highlights the complexity of the interaction of environmental chemicals with the endocrine system. Two chemicals may be metabolites of the same compound, but due to slight differences in chemical structure, have significantly different binding affinities to a hormone receptor.

 

 

 

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