Newswise — Coastal Dead Zones and other events that deplete much of the oxygen from surface waters can not only disrupt sex-hormone production in fish, but also impair the animals' reproduction, according to new research reported in the Nov. 13 Science News magazine.

In June, the magazine's senior editor, Janet Raloff, authored a two-part series on the growing incidence around the world of Dead Zones—large regions of oxygen-starved water—and new approaches to limiting the pollution that fosters them (both stories are available upon request).

"Although the hypoxia—oxygen-starved conditions—that characterize dead zones tend to drive fish away from their natural haunts, many of those fish remain around the edges of those suffocating waters, as if waiting to rush back home as soon as conditions improve," Raloff says. "While in this ecological limbo, the fish may continue to inhabit fairly oxygen-depleted waters. It made sense that this chronic oxygen deficit should impact the fish," she notes. However, during her earlier reporting, aquatic biologists noted a perplexing absence of U.S. fish kills associated with domestic Dead Zones, such as the recurrent ones that emerge every summer in the Gulf of Mexico and Chesapeake Bay.

The question then became, she says, what type of nonlethal impacts might survival in low-oxygen waters trigger.

At two new meetings, Raloff now reports, Gulf coast scientists highlight for the first time some of those nonlethal affects in wild fish: serious and significant reproductive changes. In each case, follow-up laboratory studies confirmed that the temporary hypoxia characteristic of sites where the wild fish had been studied was all it took to induce those serious reproductive impairments, which included: dramatically reduced production of eggs, poor-quality eggs and sperm, and shortened spawning cycles.

At an environmental toxicology conference, the week of Nov. 15, two of the research teams will also present laboratory data on genetic changes that appear to underlie these reproductive problems. In both cases, Raloff reports, the scientists' findings point to the involvement of a pivotal protein known as hypoxia inducible factor, or HIF. In people and other mammals, this same protein has been implicated in causing problems after oxygen flow to tissues is disrupted by heart attacks or trauma.

Raloff notes that the wild fish impacted by hypoxia in the new studies were living in shallow, sheltered coastal waters, not those animals found in open waters where the recurring Gulf Dead Zone develops. However, she points out, the degree of oxygen-deprivation experienced by the shallow, coastal fish was comparable to that found in open-water Dead Zones.

Last year, scientists in Hong Kong reported finding that in the lab, carp exposed to hypoxia produced significantly lower concentrations of certain sex hormones and impaired reproduction (March 1, 2003, Science News account—-"Sexual Hang-Up: Fish hormones change when oxygen is scarce" —is available upon request).

What's new here is that comparable reproductive impairments have now been observed in the wild. Moreover, Raloff notes, problems seen in three states with wild Gulf killifish, also known as marsh minnows, occurred despite their sex-hormone concentrations remaining fairly normal. In fact, she points out, these fish didn't even suffer constant, unremitting hypoxia. Their brief bouts of severe hypoxia occurred daily, but lasted only 2 to 3 hours.

The Nov. 13 Science News story can be accessed, beginning 6 p.m. on Nov. 12, at: http://www.sciencenews.org/articles/20041113/fob6.asp.