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Einstein researcher receives $10.8 million grant to study toxic blood reactions caused by hemoglobin
Date:9/17/2012

lular (i.e., still in the bloodstream but no longer inside red cells).

Acellular hemoglobin can initiate toxic chemical reactions and processes. This toxicity can trigger or worsen potentially serious inflammation of blood vessels that can complicate blood transfusions and has hampered development of blood substitutes.

The researchers will use the federal grant to determine the mechanisms responsible for making acellular hemoglobin toxic and to develop strategies for preventing, reducing or even reversing toxicity.

Dr. Friedman has brought together teams from Einstein, Rice, UC San Diego and the FDA to take different but complementary research approaches. Dr. Friedman and his Einstein colleagues, including Parimala Nacharaju, Ph.D. , instructor in physiology & biophysics, will study several possible strategies for neutralizing acellular hemoglobin toxicity, including the novel use of nanoparticles that release nitric oxide gas. These particles were developed at Einstein to counteract the role played by acellular hemoglobin in reducing nitric oxide levels.

The Rice/FDA team will evaluate strategies for limiting the toxic consequences of acellular hemoglobin, which include hypertension caused by reduced nitric oxide levels and damage to blood vessel walls caused by harmful chemicals called free radicals. The UC San Diego team, which includes Amy Tsai, Ph.D., and Pedro Cabrales, Ph.D., will conduct animal testing to discover the mechanisms responsible for hemoglobin-based toxicities and develop ways to reduce or eliminate them.


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Contact: Kim Newman
sciencenews@einstein.yu.edu
718-430-3101
Albert Einstein College of Medicine
Source:Eurekalert

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