With the aid of a sufur-specific flame photometric detector, an emission of volatile sulfur was detected from leaves of cucumber (Cucumis sativus L.), sqush and pumpkin (Cucurbita pepo L.), cantaloupe (Cucumis melo L.), corn (Zea mays L.), soybean (Glycine max [L.] Merr.) and cotton (Gossypium hirsutum L.). Tbe emission was studied in detai in squash and pumpkin. It

Leaf discs and detached leaves exposed to L-cysteine emitted a volatile sulfur compound which was proven by gas chromatography to be H2S. This phenomenon was demonstrated in all nine species tested (Cucumis sativus, Cucurbita pepo, Nicotiana tabacum, Coleus bbumei, Beta vulgaris, Phaseolus vulgaris, Medicago sativa, Hordeum vulgare, and Gossypium hirsutum). The emission of volatile sulfur by cucumber leaves occurred in the dark at a similar rate to that in the light. The emission of leaf discs reached the maximal rate, more than 40 picomoles per minute per square centimeter, 2 to 4 hours after starting exposure to L-cysteine; then it decreased. In the case of detached leaves, the maximum occurred 5 to 10 h after starting exposure. The average emission rate of H2S during the first 4 hours from leaf discs of cucurbits in response to 10 milimlar L-cysteine, was usually more than 40 picomoles per minute per square centimeter, i.e. 0.24 micromoles per hour per square decimeter. Leaf discs exposed to 1 milHimolar Lcysteine emitted only 2% as much as did the discs exposed to 10 millmolar L-cysteine. The emission from leaf discs and from detached leaves lasted for at least 5 and 15 hours, respectively. However, several hours after the maximal emission, injury of the leaves, manifested as chlorosis, was evdent.H2S emission was a specific consequence of exposure to L-cysteine; neither D-cysteine nor L-cystine elicited H2S emission. Aminooxyacetic acid, an inhibitor ofpyridoxal phosphate dependent enzymes, inhibited the emission.In a celi free system from cucumber leaves, H2S formation and its release occurred in response to L-cysteine. Feeding experiments with 135SIL_CyS_ teine showed that most of the sulfur in H2S was derived from sulfur in the L-cysteine supplied and that the H2S emitted for 9 hours accounted for 7 to 10% of L-cysteine taken up. 35S-labeled S032-and S042-were found in the tissue extract in addition to internal soluble S2-. These findigs suggest the existence of a sulfur cycle which converts L-cysteine to S042-through cysteine desulfhydration.Illuminated green leaves emit H2S when plants are exposed to s042- (32,35) or SO2 (6,27). Plants have the potential for reduction of s042-to a bound form of sulfide, which is incorporated into L-cysteine, by a light-driven assimilation pathway (1, 26). Therefore, the conversion of bound sulfide to free sulfide and its release as H2S is one possible origin of the H2S emitted in response to s042- (35 reductase (1,26). Still another possibility is that L-cysteine could be a precursor of H2S. L-Cysteine is a precursor ofmost organic sulfur compounds (9), and it regulates s042-uptake (13,16,29,30) Salmonella, L-cysteine is degraded to pyruvate, NH4' and sulfide by L-cysteine desulfhydrase, which is induced by L-cysteine (4,5,14,15). L-cysteine desulfhydrase activity has also been reported to exist in the XD strain of cultured tobacco cells and to be induced by L-cysteine in these cells (12). The H2S could also arise by cyanide-dependent desulfhydration of L-cyste...

4) On a scale in which the aromatic toluene peak is assignee! a value of 1000 c.p.s.; the spectrum was taken in chloroform solution with a Varían model V4300B spectrometer at 40 me. rf.(5) This structure implies no distiuction between the two possible geometrical isomers.

The relative resistance of four cultivars of the Cucurbitaceae (Cucwnis sativus L. cv. National Pickling, and inbred line SC 25; Cucurbita pepo L. cv. Prolific Straightneck Squash, and cv. Small Sugar Pumpkin) to S02 was determined. According to plots of the degree of exposure to SO2 (which depends on the SO2 concentration and the duration of the exposure), there is an 8-fold difference in resistance to this toxic gas among these cultivars. However, if the degree of injury is plotted as a function of the amount of S02 absorbed, all four cultivars appear similarly sensitive to the gas. We conclude that the principal reason for special and varietal differences in resistance among these cultivars is the relative rate of absorption of the gas. The densities of stomata on the upper and lower surfaces of leaves did not differ sufficiently between cultivars to account for the differences in absorption rates. It remains to be determined whether the differences in rate of SO2 absorption reflect differences in stomatal activity.Resistance of individual leaves changes with position on the plant axis (age of the leaf). There exists a gradient of decreasing resistance from the apex downward. This resistance gradient cannot be accounted for by differences in rates of SO2 absorption. We infer the existence of a biochemically based, developmentally controlled resistance mechanism which functions after SOs has entered the leaf. Biochemical comparisons of old and young leaves with such differences in resistance should be helpful in determining the biochemistry of SO2 toxicity.Sulfur dioxide is a naturally occurring constituent of the atmosphere. Unnaturally high concentrations of SO2 in air result from human activities, particularly combusting of fossil fuels, and these high concentrations are toxic to plants (1 1, 20, 22). Acute exposure to S02 (usually 0.1 to 10 jul/l-1 for less than 24 hr) causes necrotic lesions, but chronic exposure to somewhat lower concentrations, although injurious, does not cause necrotic lesions. Plant species and cultivars differ in the degree of injury which they sustain from the same level of acute exposure. Several investigators have attempted to quantitate these differences (8,19, 25). Most notable was O'Gara (22) who fumigated over 300 species and cultivars with SO2 and assigned to each a resistance "factor" relative to alfalfa. The SO2 exposure required to produce equivalent injury can differ as much as 15-fold between species (22). There is also evidence that cultivars within the same species can differ in resistance to SO2 (4,18 death. Heritable differences in resistance to SO2 could reflect differences in either (a) or (b). Thomas and Hill (23) showed in 1935 that the extent of injury sustained by alfalfa plants, which had been subjected to varying amounts of light and moisture in the presence of SO2, was highly correlated with the amount of S02 absorbed. Thomas (21) speculated that species differences in resistance to SO2 were mainly due to differences in the rate of absorption of SO...

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