Environmental Factor

Environmental Factor

Your Online Source for NIEHS News

January 2017

Papers of the Month

The genetics of killifish adaptation to pollution

NIEHS grantees have identified the complex genetics involved in the Atlantic killifish’s resilience to industrial contamination. The new findings are one step closer to better understanding which genes are linked with tolerance to specific chemicals and how genetic differences may affect an organism’s sensitivity to environmental contaminants.

Killifish living in four polluted East Coast estuaries have adapted to survive high levels of toxic industrial pollutants, including polychlorinated biphenyls, dioxins, and hydrocarbons. They can tolerate concentrations up to 8,000 times higher than similar killifish that are sensitive to the pollution. To better understand the genetic basis for this adaptation, the researchers sequenced the genomes of 384 individual killifish from four nonpolluted sites and compared those with killifish from polluted sites in New Bedford Harbor, Massachusetts; Newark Bay, New Jersey; Connecticut’s Bridgeport area; and Virginia’s Elizabeth River.

The genetic analysis identified hundreds of genome regions that appeared to have undergone natural selection in the pollution-resistant killifish. Several of the regions appeared in all four resistant populations and included genes involved in the previously identified aryl hydrocarbon receptor signaling pathway. These findings showed that there are likely a limited number of evolutionary paths for adaptation to pollution. Results from the new study also suggested that the genetic diversity of killifish made them unusually well-positioned to quickly adapt and survive high levels of pollution.

CitationReid NM, Proestou DA, Clark BW, Warren WC, Colbourne JK, Shaw JR, Karchner SI, Hahn ME, Nacci D, Oleksiak MF, Crawford DL, Whitehead A. 2016. The genomic landscape of rapid repeated evolutionary adaptation to toxic pollution in wild fish. Science 354(6317):1305–1308.

Researchers identify protein that triggers poison ivy itch

An NIEHS grantee and colleagues found that the immune system protein interleukin 33 (IL-33) plays a key role in triggering itch from poison ivy, the most common allergic reaction in the U.S. The new findings could lead to treatments for people allergic to urushiol, the oily sap found in poison ivy, poison sumac, and poison oak.

The researchers developed a mouse model that mimicked the skin inflammation and severe itching found in people allergic to poison ivy. Microarray analysis showed that the skin of these mice exhibited high gene expression levels of IL-33 after exposure to urushiol. The researchers then tried blocking IL-33 in the skin using an antibody that stops the processes that communicate itchy skin to the brain. Not only did the antibody reduce inflammation, but it also reduced scratching in mice with poison ivy rashes. The researchers also found they could stop the itch by blocking a receptor for IL-33, called ST2.

Although it was already known that IL-33 can induce inflammation, the new experiments showed that the protein also acts directly on nerves in the skin, exciting them and communicating itch to the brain. These findings suggest a possible alternative therapeutic approach to the current treatments of antihistamines, which typically do not stop itch, and corticosteroids, which have side effects and must be administered quickly after the exposure.

CitationLiu B, Tai Y, Achanta S, Kaelberer MM, Caceres AI, Shao X, Fang J, Jordt SE. 2016. IL-33/ST2 signaling excites sensory neurons and mediates itch response in a mouse model of poison ivy contact allergy. Proc Natl Acad Sci U S A 113(47):E7572–E7579.

New insight into telomere regulation

Research, funded in part by NIEHS, has uncovered new details about regulation of telomeres. These repeated DNA sequences protectively cap the ends of chromosomes and play an important role in cancer and aging.

Telomeres become shorter every time a cell divides. Once they are too short, telomeres send a signal for the cell to permanently stop dividing, which weakens the ability of tissues to regenerate and plays a role in many aging-related diseases. In contrast, most cancer cells show elevated levels of the telomere-lengthening enzyme, telomerase, which allows cancer cells to divide indefinitely.

To better understand what happens to telomeres damaged by oxidative stress, the researchers examined 8-oxo-7,8-dihydro-2'-deoxyguanine (8-oxoG), a common DNA lesion caused by oxidative stress. The research revealed that when a nucleotide containing 8-oxoG was incorporated into a telomere, any further elongation stopped. By contrast, 8-oxoG lesions found within the telomeric DNA promoted telomerase activity and telomere elongation. These findings showed the mechanism by which the 8-oxoG lesion arises in telomeres dictates whether telomerase is inhibited or stimulated and, thus, determines whether the telomere is shortened or lengthened.

The information revealed by this study could be useful for developing new ways to fight cancer and therapies that could help lessen the effects of aging.

CitationFouquerel E, Lormand J, Bose A, Lee HT, Kim GS, Li J, Sobol RW, Freudenthal BD, Myong S, Opresko PL. 2016. Oxidative guanine base damage regulates human telomerase activity. Nat Struct Mol Biol 23(12):1092–1100.

Prenatal lead linked with stunted growth in early childhood

NIEHS grantees and colleagues reported an association between higher maternal blood levels during the third trimester of pregnancy and stunted growth in their children. The study, conducted in Mexico, adds to previous findings linking lead with decreased stature and weight in early childhood.

The new study involved participants in the NIH-funded Programming Research in Obesity, Growth, Environment and Social Stressors cohort in Mexico City. To determine how lead exposure during pregnancy is associated with children's growth, the researchers collected blood lead levels in the second and third trimesters of pregnancy, as well as at delivery. They also assessed the bone lead levels of the mothers as a long-term exposure marker. The researchers measured the height, weight, body mass index, and percentage body fat of the participants’ children 4 to 6 years after the prenatal lead exposure.

The researchers found that higher levels of maternal blood lead during the third trimester were significantly associated with decreased height and weight in the 4- to 6-year-old children. Ongoing follow-up and longitudinal analyses are needed to determine how stunted growth in early childhood affects the children’s overall growth trajectory and other health outcomes.

CitationRenzetti S, Just AC, Burris HH, Oken E, Amarasiriwardena C, Svensson K, Mercado-Garcia A, Cantoral A, Schnaas L, Baccarelli AA, Wright RO, Tellez-Rojo MM. 2017. The association of lead exposure during pregnancy and childhood anthropometry in the Mexican PROGRESS cohort. Environ Res 152:226–232.

(Nancy Lamontagne is a science writer with MDB Inc., a contractor for the NIEHS Division of Extramural Research and Training.)

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