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PubMed1974

Inhibition of the photosynthetic capacity of isolated chloroplasts by ozone.

Isolated spinach chloroplasts have been used as a model system for studying the interaction of ozone, a component of photochemical smog, with plant membranes. Ozone bubbled into a suspension of isolated chloroplasts inhibits electron transport in both photosystems without uncoupling ATP production. Photosystem I (reduced 2,6-dichlorophenolindolphenol --> NADP(+)) is a little more sensitive than photosystem II (H(2)O --> 2,6-dichlophenolindolphenol). Ozone does not act as an energy transfer inhibitor, since the drop in ATP production and high energy intermediate (measured by amine-induced swelling) is nearly parallel to the decline in electron transport. A reasonable hypothesis is that ozone disrupts the normal pathway of energy flow from light-excited chlorophyll into the photoacts by a disruption of the components of the membrane but not a general disintegration of the membrane. In addition, ozone does not seem to penetrate into the grana region through the outer membrane of intact plastids, since ozone lowers the bicarbonate-supported O(2) evolution but does not affect the rate of ferricyanide reduction in the same plastids after osmotic disruption. This would indicate that the effect of ozone on green plants, at low concentrations, may be due to the interaction of ozone with the first membrane it contacts and not directly with internal metabolic processes.

Journal Article↗
PubMed1975

Ozone-induced Loss of Intracellular Potassium Ion from Chlorella sorokiniana.

The unicellular algae Chlorella sorokiniana was used as a model system to investigate the interaction of ozone with plant cell membranes. Ozone induces K(+) leakage from Chlorella sorokiniana similar to the electrolytic loss observed from many higher plants under stressful conditions. The kinetics of this leakage indicate that ozone initially interacts reversibly (within sec) with sites on membranes allowing a passive efflux of K(+). This efflux ceases within minutes after the ozone stress is removed. This return to normal efflux is very temperature dependent. High intracellular osmolarity seems to be an important criterion of susceptibility to ozone injury in this model system, since rates of ozone-induced K(+) leakage are less when the external osmotic potential is decreased by suspension of the cells in mannitol. Cell interaction with ozone is further complicated by a saturating-type dependence of the K(+) efflux upon ozone concentration within the medium.

Journal Article↗
PubMed1982

Ozone Inhibition of Photosynthesis in Chlorella sorokiniana.

Exposure of Chlorella sorokiniana (07-11-05) to ozone inhibits photosynthesis. In this study, the effects of ozone on O(2) evolution and fluorescence yields are used to characterize this inhibition. At an ozone dose of about 3 micromoles delivered to 2 x 10(9) cells, the photosynthetic rate of the cells is inhibited 50%, as indicated by a decrease in bicarbonate-stimulated O(2) evolution (control rate, 1.4 +/- 0.3 x 10(-15) moles per cell per minute).Normal patterns of chlorophyll fluorescence are also altered. Upon continuous exposure to ozone (3.5 x 10(-7) moles O(3) per minute), three stages of change in relative fluorescence yields are observed: (a) a rise in variable yield with no corresponding change in nonvariable yield (after 1-2 minutes), which was interpreted to be a shift in the energy flow pathway; (b) a decline in variable yield with a slight rise in nonvariable yield (requiring 3-5 minutes), interpreted to be a blockage in the CO(2) fixation pathways; and (c) complete blockage of variable yield with a concurrent decline in nonvariable yield (8-10 minutes), interpreted to be a destruction of the pigment system. The timing of each stage depended upon the ozone concentration and its delivery rate to the cell suspension. These results are compared with ozone-induced decline in photosynthesis and leaf water potential changes reported for other plant systems.Evidence is also presented to suggest that ozone effects on the photosynthetic processes are attributable to ionic imbalances brought about by ozone interaction with the plasmalemma rather than a direct effect on the chloroplast.

Journal Article↗
PubMed1985

Water Stress Reduces Ozone Injury via a Stomatal Mechanism.

Various studies have shown that water-stressed plants are more tolerant of ozone exposures than are unstressed plants. Two probable explanations for this tolerance are (a) stomatal closure which reduces ozone uptake and (b) biochemical or anatomical changes within the leaves. Phaseolus vulgaris cv Pinto bean plants were established and transferred to membrane systems which controlled the osmotic potential around the roots at -35 or -80 kilopascals for 5 days prior to ozone treatment (0 or 1.0 microliters per liter for 2 hours). Both water-stressed and unstressed plants were sprayed with various concentrations of abscisic acid to close the stomata or with fusicoccin to induce stomata opening. The abaxial stomatal resistances of primary and trifoliate leaves were measured just prior to ozone exposure. Plant response to ozone was determined by stress ethylene production and chlorophyll loss. Both water stress and abscisic acid induced stomatal closure and reduced ozone injury. In water-stressed plants, fusicoccin induced stomatal opening and those plants were as sensitive to ozone as were the non-water-stressed plants. These data suggest that water stress protects plants from ozone injury mainly through its influence on stomatal aperture rather than through biochemical or anatomical changes.

Journal Article↗
PubMed2001

Direct-Sun column ozone retrieval by the ultraviolet multifilter rotating shadow-band radiometer and comparison with those from Brewer and Dobson spectrophotometers.

A methodology for direct-Sun ozone retrieval using the ultraviolet multifilter rotating shadow-band radiometer (UV-MFRSR) is presented. Total vertical column ozone was retrieved in three stations: Mauna Loa, Hawaii, in the U.S., and Regina, Saskatchewan, and Toronto, Ontario, in Canada, from direct solar irradiances of the UV-MFRSR at 325-, 305-, 332-, and 311-nm channels (2-nm FWHM). The total uncertainty of ozone retrievals in this study is +/-2.0%. For Mauna Loa the mean ratios of the UV-MFRSR column ozone retrievals to the collocated Dobson and Brewer were 0.998 and 0.986 between May and September of 1999. The mean ratio of UV-MFRSR retrievals to the collocated Brewer retrievals was 1.012 in Toronto between April and August of 1999, and the mean ratio of retrievals of the UV-MFRSR to the collocated Brewer was 0.988 in Regina between June and September of 1999. Total vertical column ozone values for solar zenith angles of >70 degrees were not considered, because of the signal-to-noise ratio and the angular response of the instruments, and were not used in the evaluation. The advantages of total vertical column ozone retrieval using UV-MFRSR include relatively low cost, computer-controlled operation, automated calibration stability checks, and minimal maintenance. It allows for the real-time measurement of total vertical column ozone. The UV-MFRSR is being used at 28 sites across the United States and 2 sites in Canada that form the U.S. Department of Agriculture UV-B Radiation Monitoring and Research Program. This constitutes a unique network of total vertical colunm ozone measurement.

Journal Article↗
PubMed1963

EFFECT OF OZONE ON SURVIVAL AND PERMEABILITY OF ESCHERICHIA COLI.

Scott, D. B. McNair (University of Pennsylvania, Philadelphia) and E. C. Lesher. Effect of ozone on survival and permeability of Escherichia coli. J. Bacteriol. 85:567-576. 1963.-Escherichia coli cultures in the logarithmic phase or resting were treated with various concentrations of ozone in saline solution. Approximately 2 x 10(7) molecules of ozone per bacterium killed 50% of the cells. Ozone caused leakage of cell content into the medium, and lysis of some cells. Low concentrations of ozone did not react with the glutathione within the cells, although reaction with glutathione in solution was immediate and stoichiometric. The effect on nucleic acid within the cells was to change the solubility and to cause the release of ultraviolet-absorbing material into the medium. Ozone attacked the ring structure of the base or the carbohydrate only when the substance was in the medium. Nucleic acids released into the medium were reabsorbed by cells which were not lysed. Viable cells resumed growth immediately, and grew at rates determined by the nutrients either added to the medium or which resulted from leakage and lysis of nonviable cells. It is postulated that the primary attack of ozone was on the cell wall or membrane of the bacteria, probably by reaction with the double bonds of lipids, and that leakage or lysis of the cells depended on the extent of that reaction.

Bacteria↗
PubMed2004

Ozone and short-term mortality in 95 US urban communities, 1987-2000.

CONTEXT: Ozone has been associated with various adverse health effects, including increased rates of hospital admissions and exacerbation of respiratory illnesses. Although numerous time-series studies have estimated associations between day-to-day variation in ozone levels and mortality counts, results have been inconclusive. OBJECTIVE: To investigate whether short-term (daily and weekly) exposure to ambient ozone is associated with mortality in the United States. DESIGN AND SETTING: Using analytical methods and databases developed for the National Morbidity, Mortality, and Air Pollution Study, we estimated a national average relative rate of mortality associated with short-term exposure to ambient ozone for 95 large US urban communities from 1987-2000. We used distributed-lag models for estimating community-specific relative rates of mortality adjusted for time-varying confounders (particulate matter, weather, seasonality, and long-term trends) and hierarchical models for combining relative rates across communities to estimate a national average relative rate, taking into account spatial heterogeneity. MAIN OUTCOME MEASURE: Daily counts of total non-injury-related mortality and cardiovascular and respiratory mortality in 95 large US communities during a 14-year period. RESULTS: A 10-ppb increase in the previous week's ozone was associated with a 0.52% increase in daily mortality (95% posterior interval [PI], 0.27%-0.77%) and a 0.64% increase in cardiovascular and respiratory mortality (95% PI, 0.31%-0.98%). Effect estimates for aggregate ozone during the previous week were larger than for models considering only a single day's exposure. Results were robust to adjustment for particulate matter, weather, seasonality, and long-term trends. CONCLUSIONS: These results indicate a statistically significant association between short-term changes in ozone and mortality on average for 95 large US urban communities, which include about 40% of the total US population. The findings indicate that this widespread pollutant adversely affects public health.

Air Pollution↗
PubMed2004

Corona discharge influences ozone concentrations near rats.

Ozone can be produced by corona discharge either in dry air or when one electrode is submerged in water. Since ozone is toxic, we examined whether ozone production by corona near laboratory animals could reach levels of concern. Male rats were exposed to a corona discharge and the concentration of ozone produced was measured. The resulting concentration of ozone ranged from ambient levels to 250 ppb when animals were located 1 cm from a 10 kV source. Similar ozone concentrations were observed when a grounded water source was present. Possible explanations for, as well as concerns regarding, ozone production under these conditions are discussed.

Air Pollution↗
PubMed1992

Ozone is mutagenic in Salmonella.

Ozone is a highly reactive gas that has been tested for genotoxicity in a number of systems. Induced genetic damage resulting from ozone treatment may not be readily observed because of the high toxicity of the chemical and difficulties in generating and administering controlled concentrations. The mutagenicity of ozone was investigated in Salmonella typhimurium using a plate test protocol designed for reactive vapours and gases. Ozone, at two to three consecutive doses, induced weak, albeit statistically significant, mutagenic responses in tester strain TA102 with and without Aroclor-induced rat liver S9 (lowest effective mean concentration of 0.019 ppm; 35 min total exposure). However, dose-related responses were not always obtained. No mutagenicity was detected in strains TA98, TA100, or TA1535, with or without S9. In strain TA104, ozone induced a weak response only at a single dose with S9; this response was not reproducible. Mutagenicity was dependent on the ozone flow rate and total exposure time, with variations in the optimum dose-time regimen leading to toxicity or complete inactivity. The data show that ozone is a very weak bacterial mutagen and only when tested under narrowly prescribed, subtoxic dosing conditions.

Animals↗
PubMed1994

Ozone increases amino- and carboxy-terminal atrial natriuretic factor prohormone peptides in lung, heart, and circulation.

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic peptides may mediate both of these effects in that they increase pulmonary capillary permeability resulting in edema formation and are potent vasodilating peptides. To examine this possibility, the lungs of Fischer 344 rats were exposed to ozone (0.5 ppm) for 8 hours which resulted in a three- to fourfold increase in atrial natriuretic peptides. Ozone also increased atrial natriuretic peptides in the heart two- to fivefold from 266 +/- 25, 226 +/- 22, and 288 +/- 40 ng/g (room air) to 716 +/- 26, 471 +/- 14, and 1473 +/- 235 ng/g recognized by the proANFs 1-30 and 31-67 and atrial natriuretic factor radioimmunoassays, respectively. Ozone also doubled the concentrations of pro-ANFs 1-30, 31-67, and 1-98 and ANF in the circulation. This study demonstrates that ozone increases atrial natriuretic peptides within the heart, lung, and circulation, suggesting that atrial natriuretic peptides may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure. Since the proANF 31-67 radioimmunoassay exclusively recognizes the ANF prohormone within the heart, this study further indicates that ozone can increase the synthesis of the ANF prohormone.

Animals↗
PubMed1994

Acute effects of ambient ozone on respiratory function of Swiss schoolchildren after a 10-minute heavy exercise.

This study was conducted in Switzerland between May and October 1989 to assess possible decrements in lung function occurring as a result of 10 minute exposure to ambient air containing different ozone concentrations. Once a month, 128 children in two different areas of Southern Switzerland (Chiasso and Aurigeno) had a pulmonary function test before and after a standardized 10 minute exercise (pulse rate, 170/min) on a cycle ergometer, outdoors. Ozone concentrations were similar in both areas, ranging from 40 to 157 micrograms/m3 (1/2h means) during the exercise tests. The two communities differed with respect to long-term average pollution levels. The mean NO2 concentration over the six months study period was 70 micrograms/m3 in Chiasso and 18 micrograms/m3 in rural Aurigeno. Of the eligible children 85% participated and attended 4-6 tests. Parents completed a standardized questionnaire on family background, home characteristics and the child's early and present illness history. A total of 500 acceptable pairs of spirograms and corresponding ozone concentrations (average 3.8 per child) were available for analysis. Regressions of each individual's pre-post differences of FVC, FEV1 and peak flow on ozone concentrations measured during the outdoor exercise indicated that elevated ozone levels significantly reduced peak flow values. Adjustments for temperature and relative humidity increased the magnitude of the peak flow slopes. The average adjusted regression coefficient for delta-peak flow on ozone was -2.28 mL/s/micrograms/m3 (95% CI, -0.57 -3.99). It is noteworthy that the observed relationships occurred at ozone concentrations below 160 micrograms/m3 and after an exercise duration of only 10 minutes.

Atmosphere↗
PubMed1998

Toxicity of ozone to fish larvae and Daphnia magna.

Ozone can be used as an alternative to chlorination to control biofouling in cooling water systems. The possible negative environmental impact of a discharge of ozone-containing cooling water was investigated. The acute toxicity of dissolved ozone was determined for fish larvae of three species [Cyprinus carpio (at 27 degrees C), Leuciscus idus (at 27 degrees C) and Clarias gariepinus (at 32 degrees C)] and to Daphnia magna (at 21 and 27 degrees C). The results indicate that ozone is very harmful to aquatic life. Daphnids are more sensitive to ozone than fish larvae. The mean 48-h LC50 value for the larvae amounts to about 35 microg/liter, while the 48-h NOEC for D. magna was 11 microg/liter (at 21 degrees C). It was concluded that, to protect aquatic life, discharged cooling water should not contain any dissolved ozone. This can be achieved in practice by mixing the treated cooling water with a source of organic substances before discharge, as free ozone will react immediately with organic matter and thus disappear.

Animals↗
PubMed1994

Ozone effects on mechanics and arachidonic acid metabolite concentrations in isolated rat lungs.

In whole animals, ozone acutely impairs pulmonary function, an effect which may be mediated by eicosanoids. This study determined if the lung itself, separated from blood components and the CNS, responds to ozone with increased eicosanoid production and decreased function. Wistar rat lungs were placed in a negatively ventilated, buffer-perfused, isolated system, where they were exposed to filtered air or 1 ppm ozone for 3 hr. Ozone increased lung resistance (P = 0.02) and decreased dynamic compliance (P = 0.003, multivariate ANOVA for repeated measures). Pulmonary artery pressure, lung weight/body weight, and cells in lung lavage (BALF) did not change. In the perfusate, ozone increased the concentration of 6-keto-PGF1 alpha, PGF2 alpha, PGD2, and TxB2 (all P < 0.05, t test) but not LTC4/D4 or PGE2. In BALF, ozone did not change the concentrations of any of the arachidonic acid metabolites tested (PGE2, 6-keto-PGF1 alpha, PGD2, or LTC4/D4). We conclude that ozone increased intravascular concentrations of some cyclooxygenase products in the isolated buffer-perfused lung, an effect associated with reduced lung function.

Animals↗
PubMed1995

Temperature, ambient ozone levels, and mortality during summer 1994, in Belgium.

The number of daily deaths, temperature, relative humidity, and 24-hr concentrations of main air pollutants observed during a heat wave (June 27-August 7, 1994) in Belgium were compared with those recorded before and after this heat wave. All these variables were averaged over the country. Expected mortality was calculated from daily deaths observed during the summers of 1985-1993. The influence of meteorological and air pollution variables on daily mortality was analyzed using generalized least-squares method. Mortality recorded during the heat wave was higher than expected: it increased by 9.4% in the age group 0-64 years (236 excess deaths; P < 0.001) and by 13.2% in the elderly (1168 excess deaths; P < 0.001). After the heat wave, mortality in the elderly was lower than expected (178 deficit deaths; P< 0.05); the net excess of mortality in the whole population amounted to 1226 deaths when accounting for this deficit. This increased mortality was associated with unusually high outdoor temperatures (range of daily mean: 15.3-27.5 degrees C) and elevated ozone levels (range of 24-hr concentration: 34.5-111.5 microg/m3). The duration of the ozone overexposure during the heat wave was also uncommon: half-hour concentrations of ozone exceeded, on an average, 100 microg/m3 for 8 consecutive hr. The number of daily deaths was mostly correlated with the mean daily temperature and 24-hr ozone concentration, both measured the day before. A synergy between temperature and ozone in their effects on mortality was also highlighted in both age groups. The product of the logarithm of temperature by the logarithm of ozone concentration, both measured the day before, contributed to 39.5% of the variance of the logarithm of daily deaths in elderly and to 4.5% in the age group 0-64 years. In conclusion, elevated outdoor temperatures combined with high ozone concentrations were assumed to be the likely cause of the important excess mortality observed in Belgium during the summer, 1994.

Adolescent↗
PubMed1997

Association between ozone and hospitalization for respiratory diseases in 16 Canadian cities.

The effects of tropospheric ozone on lung function and respiratory symptoms have been well documented at relatively high concentrations. However, previous investigations have failed to establish a clear association between tropospheric ozone and respiratory diseases severe enough to require hospitalization after controlling for climate, and with gaseous and particulate air pollution at the lower concentrations typically observed in Canada today. To determine if low levels of tropospheric ozone contribute to hospitalization for respiratory disease, air pollution data were compared to hospital admissions for 16 cities across Canada representing 12.6 million people. During the 3927-day period from April 1, 1981, to December 31, 1991, there were 720,519 admissions for which the principle diagnosis was a respiratory disease. After controlling for sulfur dioxide, nitrogen dioxide, carbon monoxide, soiling index, and dew point temperature, the daily high hour concentration of ozone recorded 1 day previous to the date of admission was positively associated with respiratory admissions in the April to December period but not in the winter months. The relative risk for a 30 ppb increase in ozone varied from 1.043 (P < 0.0001) to 1.024 (P = 0.0258) depending on the selection of covariates in the regression model and subset of cities examined. The association between ozone and respiratory hospitalizations varied among cities, with relative risks ranging from 1.000 to 1.088 after simultaneous covariate adjustment. Particulate matter and carbon monoxide were also positively associated with respiratory hospitalizations. These results suggest that ambient air pollution at the relatively low concentrations observed in this study, including tropospheric ozone, is associated with excess admissions to hospital for respiratory diseases in populations experiencing diverse climates and air pollution profiles.

Air Pollutants↗
PubMed1997

Modulation of the inflammatory effects of inhaled ozone in rats by subcutaneous prolactin-secreting, pituitary-derived tumors.

Rats are more sensitive to ozone-induced pulmonary inflammation and damage during late pregnancy and throughout lactation than in pre- or early pregnancy or postlactation. This window of sensitivity coincides with a period of elevated levels of pituitary-derived prolactin or placental lactogen. In this study, we investigated the hypothesis that prolactin exerts an enhancing effect on ozone-induced pulmonary inflammation and damage, thus presenting a plausible explanation for the sensitivity profile observed in rats. Hyperprolactinemia was achieved by using rats with subcutaneous tumors that were derived from the MMQ tumor model previously described by Adler and co-workers (Adler, R. A., Krieg, R. J., Farrell, M. E., Deiss, W. P., and MacLeod, R. M., Metabolism 40, 286-291, 1991). A variant of the MMQ tumor, the MMQr tumor, which appeared spontaneously from a single passage of MMQ tumor tissue, produced elevated levels of corticosterone in addition to high levels of prolactin. These two subcutaneous tumors had markedly different effects on adrenal, thymus, and spleen weights because of the different hormonal milieu they generated. There was also a significant difference between MMQ- and MMQr-bearing rats in their inflammatory response to acute ozone exposure as assessed by polymorphonuclear leukocytes (PMNs) in the airways. Rats with MMQ tumors were not significantly different from non-tumor-bearing controls in their baseline level of airway PMNs and PMN inflammation following ozone exposure, whereas MMQr-bearing rats had significantly elevated baseline PMNs in their airways and a greater PMN response to inhaled ozone. The hormonal milieu and elevated PMNs in the airways of both unexposed and ozone-exposed rats with MMQr tumors were similar to levels observed in lactating rats. The role of corticosterone in pulmonary inflammation in this model was investigated further by treating MMQ tumor-bearing rats with dexamethasone. Dexamethasone was effective in producing changes in organ weights similar to those observed in MMQr rats, but did not elicit higher airway PMN concentrations in unexposed rats as observed in the MMQr rats. We conclude that in this animal model prolactin did not significantly elevate airway PMN inflammation induced by ozone, and supplementation with exogenous glucocorticoid did not duplicate the endogenous airway PMNs numbers observed in MMQr-bearing rats or lactating rats.

Administration, Inhalation↗
PubMed2001

Ozone treatment reduces markers of oxidative and endothelial damage in an experimental diabetes model in rats.

Ozone has been used as a therapeutical agent and beneficial effects have been observed. However so far only a few biochemical and pharmacodynamic mechanisms have been elucidated. We demonstrate that controlled ozone administration may promote an oxidative preconditioning or adaptation to oxidative stress, preventing the damage induced by reactive oxygen species (ROS). Taking into account that diabetes is a disorder associated with oxidative stress, we postulate that ozone treatment in our experimental conditions might protect antioxidant systems and maintain, at a physiological level, other markers of endothelial cell damage associated with diabetic complications. Five groups of rats were classified as follows: (1) control group treated only with physiological saline solution; (2) positive control group using streptozotocin (STZ) as a diabetes inductor; (3) ozone group, receiving 10 treatments (1.1 mg kg(-1)), one per day after STZ-induced diabetes; (4) oxygen group (26 mg kg(-1)), one per day, as in group 3 but using oxygen only; (5) control ozone group, as group 3, but without STZ. The ozone treatment improved glycemic control and prevented oxidative stress, the increase of aldose reductase, fructolysine content and advanced oxidation protein products. Nitrite and nitrate levels were maintained without changes with regard to non-diabetic control. The results of this study show that repeated administration of ozone in non-toxic doses might play a role in the control of diabetes and its complications.

Animals↗
PubMed2000

Effect of respiratory pattern on ozone injury to the airways of isolated rat lungs.

Ozone stimulates the "defensive" C-fibers in the lungs, changing breathing pattern to rapid and shallow. We hypothesized that when ozone is administered to the isolated lung with a rapid shallow breathing pattern rather than a slow deep pattern, relatively less airway epithelial damage would occur. Four groups of isolated buffer perfused rat lungs were exposed to ozone (1 ppm) or to filtered air for 90 min with either a slow deep (SDB, tidal volume 2.4 ml, frequency 40 breaths/min) or a rapid shallow breathing pattern (RSB, tidal volume 1.2 ml, frequency 80 breaths/min), resulting in an equivalent inspired dose. The absorbed dose of ozone did not differ between the exposed groups. Ethidium homodimer-1 was then instilled into the trachea to identify injured airway epithelial cells. The lungs were fixed, the airways were microdissected, and the airway epithelial cells were counterstained with YPRO-1 prior to evaluation with confocal microscopy. Ozone-induced airway epithelial cell injury occurred to a lesser overall degree when lungs were exposed by the RSB pattern (p = 0.003). The relative reduction in injury was greater (p < 0.05) in the proximal axial airway than in its adjacent airway branch and terminal bronchioles. Ozone induced an increase in pulmonary resistance with the SDB pattern but not with the RSB pattern. Thus, at an equivalent dose of inspired ozone, a RSB pattern resulted in less total damage than a SDB pattern and the distribution of protection was heterogeneous with proximal axial airways displaying the greatest relative reductions in epithelial damage.

Animals↗