Editor's note: Science Scan is a roundup of recently published biotechnology-relevant research.

People who follow the news are aware of the ozone layer in the upper atmosphere, which shields the earth from the sun's blistering ultraviolet radiation.

Ozone (O₃) is an unstable bluish gas with a pungent, irritating odor. It's formed in the air by lightning and on the ground in automobile engines, among other sources. O₃ is used industrially to purify drinking water, treat industrial waste and as an oxidizing agent in many chemical processes. Now the controversial molecule is being nominated for an antipathogenic portfolio.

An article in Sciencexpress dated Nov. 14, 2002, bears the title: "Evidence for antibody-catalyzed ozone formation in bacterial killing and inflammation." Its authors are chemists and immunologists at the Scripps Research Institute in La Jolla, Calif.

They have found that ozone and hydrogen peroxide (H₂O₂), produced by the body's immune system, can efficiently kill bacteria. Antibodies, their paper reports, catalyze the production of peroxide from "singlet oxygen" - an excited state of the molecule - and water. The water-oxidation pathway may begin by triggering immune system neutrophils, which park antibodies on their cell surface, and generate singlet oxygen when activated.

An editorial accompanying the Science paper makes the point, "Antibodies have long been known as the immune system's reconnaissance forces: scouts that seek out foreign antigens and summon up the big guns to wipe them out. But evidence now indicates that antibodies may also be killers in their own right."

An in vitro experiment demonstrated that antibodies - together with a singlet oxygen-generating setup that couldn't kill bacteria on its own - wiped out more than 95 percent of Escherichia coli bacteria, with ozone as key bug killer. Extending their work to in vivo experiments, the researchers showed that inflammatory reactions they provoked in the skin of rats "contains an oxidant with the chemical signature of ozone."

The paper concluded: "The results presented here may be biologically significant in terms of the role of the immune system in both defense and its counterpart, induction of disease. . . . This is the first direct evidence that [antibodies] can destroy their antigenic targets in the absence of complement or phagocytes."

Treating Ongoing Symptoms Of Asthma Thrice As Efficacious As Rote Official Treatment Guidelines

A study in The Lancet dated Nov. 30, 2002, indicates that targeting the underlying cause of asthma - rather than treating symptoms of the disorder - could be more effective in reducing severe asthmatic attacks. The paper is titled: "Asthma exacerbation and sputum eosinophil counts: A randomized controlled trial." Its authors are at the Glenfield Hospital in Leicester, UK.

They randomly allocated 74 patients with moderate to severe asthma to management by either prescribed British asthma guidelines or by normalization of their induced sputum eosinophil cell counts. The latter cohort had corticosteroid medication (oral or inhaled) regulated in response to eosinophil changes as the study progressed. The sputum eosinophil level was 63 percent lower over 12 months among sputum-management patients than those receiving conventional therapy. The former contingent suffered only 35 severe asthma attacks vs. 105 who received the standard treatment.

Estrogen Replacement Given To Postmenopausal Women Provides No Help For Cognitive Function

Some controversy surrounds potential risks and benefits of estrogen replacement therapy given postmenopausal women. A controlled clinical trial invited 2,763 subjects with coronary disease to enroll in the cognitive function substudy. It is reported in The American Journal of Medicine published Nov. 21, 2002. The title: "Effect of postmenopausal hormone therapy on cognitive function: The heart and estrogen/progestin replacement study." Its authors in the multicenter trial are at the University of California at San Francisco and associated VA Medical Center, the University of California at San Diego and Wyeth-Ayerst Research.

Subjects were followed for more than four years, with cognitive function measured in 517 women in the hormone group and 546 in the placebo contingent. Treatment with oral estrogen plus progestin therapy over the four years did not result in better cognitive function compared with treatment by placebo in elderly women with coronary disease. Clinical trials are currently in progress to determine if estrogen therapy reduces the risk of developing Alzheimer's disease and other forms of dementia.

Gene Embedded In DNA Stretch Casts Light On Neurodegeneration in Parkinson's Disease

A joint Dutch/Italian research team has identified a genetic mutation linked with early onset Parkinson's disease (PD). Their report in Sciencexpress dated Nov. 22, 2002, is titled: "Mutations in the DJ-1 gene associated with autosomal recessive early onset parkinsonism." The paper's co-authors are at La Sapienza University in Rome and Nijmegen University in the Netherlands.

Although the function of the protein that the gene encodes remains unknown, some evidence suggests that it helps protect cells against oxidative damage. In a previous study of two families prone to early onset PD, the co-authors identified a stretch of DNA called PARK7 along a certain chromosome associated with the disorder. Both families, one Dutch, the other Italian, live in genetically isolated communities in the Netherlands and Italy, respectively. Now the team has homed in on the DJ-1 gene within the PARK7 sequence. Mutations in this gene caused the DJ-1 protein to be missing in the Dutch family, and functionally inactive in the Italian pedigree. The authors suggest that this loss of function leads to neurodegeneration, and that further investigation of the protein's role in the process may enhance understanding of how PD develops.