Ethylene is one of the simplest organic molecules, yet it has remarkably different meanings in plants and animals. I first became interested in ethylene during my predoctoral years because of its familiar role in fruit ripening. My interest took a different direction during my early research years at Louisiana State University and later at Southern University, when I began examining how ethylene may arise through oxidative chemistry and its possible significance in the biomedical sciences. The same molecule can therefore tell two very different biological stories.
A regulated hormone in plants
Although it took decades of research to understand the process, plants are now known to possess a dedicated and tightly regulated pathway for ethylene biosynthesis and signaling.
Methionine is first converted to S-adenosylmethionine and then to 1-aminocyclopropane-1-carboxylic acid, commonly known as ACC, before the final formation of ethylene. Adams and Yang’s identification of ACC as the intermediate linking methionine to ethylene was a decisive step in mapping this pathway.
Once produced, ethylene is recognized through specialized receptors and signaling pathways. The identification of the Arabidopsis ETR1 gene helped explain how plants perceive ethylene and translate its presence into coordinated biological responses.
Ethylene regulates fruit ripening, senescence, abscission, seed germination, growth, development, and responses to environmental stress. Its importance in fruit ripening was recognized well before the details of its biosynthetic and signaling pathways were known.
Because ethylene is a gas, its influence is not necessarily confined to the tissue in which it is produced. It can move through surrounding air spaces and affect nearby fruits and plant tissues. This gives ethylene importance not only within an individual plant but also in crop production, harvesting, storage, transportation, and postharvest management.
Long before the chemistry was understood, people had learned to make practical use of its effects. Historical accounts describe the burning of incense in enclosed rooms in ancient China to hasten the ripening of pears. In the 1920s, researchers observed that warming citrus fruit with kerosene heaters in enclosed spaces caused peel degreening that could not be explained by heat alone. The effect was subsequently attributed to ethylene present in the combustion gases.
Understanding and controlling ethylene has enormous economic importance. Ethylene production, exposure, and perception influence fruit ripening, color, firmness, storage, transportation, shelf life, market quality, and postharvest losses. Better management of ethylene can help coordinate harvesting, preserve agricultural produce, and reduce unnecessary chemical interventions.
That economic importance can also create incentives for crude and potentially unsafe shortcuts. One troubling example is the use of calcium carbide to hasten fruit ripening. When calcium carbide is placed in or near fruit crates or ripening rooms, it reacts with moisture to release acetylene, not ethylene. Acetylene can nevertheless mimic some of ethylene’s ripening effects. Unlike controlled treatment with ethylene gas, the use of calcium carbide is prohibited in India because of its potential health risks. The Food Safety and Standards Authority of India has called for inspections of fruit markets, storage facilities, wholesalers, and distributors to prevent its use.
Ethylene as a product of oxidative chemistry in animals
Animals, including humans, do not appear to possess a comparable endogenous ethylene hormone or receptor-mediated signaling system. Instead, ethylene may be generated during oxidative processes, including lipid peroxidation and the oxidation of methionine-related compounds.
My interest in this question has roots in the early free-radical literature and in my association with the late Professor William A. Pryor. The issue was not simply whether oxidative systems could produce ethylene, but which oxidants were actually responsible.
One of the early mechanistic studies was reported by Charles Beauchamp and Irwin Fridovich in 1970. They demonstrated ethylene formation from methional in a xanthine-xanthine oxidase system and proposed that hydroxyl radical was responsible for the transformation. Their work helped establish methional-derived ethylene as a probe for studying oxygen-radical reactions.
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Later, Pryor, Jin, and Squadrito examined the peroxynitrite-mediated oxidation of methionine and its analog, 2-keto-4-methylthiobutyric acid (KTBA). They showed that the reactions could follow competing pathways: a two-electron pathway producing the corresponding sulfoxide and a one-electron pathway ultimately producing ethylene. These studies provided an important chemical foundation for considering ethylene as a product of oxidative reactions in biological systems.
The biomedical relevance of this chemistry was illustrated in an experimental study in rats. Following intragastric administration of ferrous sulfate, hydroxyl-radical-like activity was assessed through the conversion of KTBA to ethylene. Ascorbic acid, which is often combined with oral iron to help maintain iron in a reduced and more readily absorbable form, exerted concentration-dependent effects in vitro, enhancing ethylene formation at lower concentrations while suppressing it at higher concentrations. In the corresponding animal experiments, its radical-scavenging action was more prominent. These findings underscore the complex redox chemistry that can accompany iron administration, particularly when some of the administered iron remains unabsorbed in the gastrointestinal tract.
Ethylene has also been detected in exhaled breath, including in humans. A controlled human study found increased breath ethylene during experimentally induced systemic inflammation. Its presence may therefore provide information about oxidative activity and could have value as a noninvasive indicator of oxidative stress. Considerably more work is needed, however, before breath ethylene can be regarded as a validated clinical biomarker.
Which radical oxidant is responsible?
This question remained with me: What is the actual one-electron oxidant responsible for ethylene formation in peroxynitrite reactions?
Before the importance of carbon dioxide in peroxynitrite chemistry was fully recognized, ethylene formation had been attributed to an undefined activated intermediate of peroxynitrous acid, sometimes represented as ONOOH*. With advances in peroxynitrite chemistry, it became reasonable to ask whether this elusive oxidant might instead be carbonate radical, nitrogen dioxide, or some combination of the two.
The work presented in my 2023 Society of Toxicology poster, “On the Nature of Free Radical Oxidant(s) Responsible for Ethylene Production in Peroxynitrite-CO2 Reactions with Methionine and Its Analogs,” examined ethylene formation during reactions of peroxynitrite with methionine, KTBA, and selenomethionine. The reactions were performed in sealed vials, and ethylene in the headspace was measured by gas chromatography with flame-ionization detection.
The substrates behaved very differently. Using the ethylene yield from KTBA as 100 percent, the relative yields from methionine and selenomethionine were only about 14 percent and 1 percent, respectively. Decomposed peroxynitrite produced no detectable ethylene, confirming that active oxidant chemistry was required.
One result was particularly interesting. For a given substrate, ethylene production was essentially similar whether or not bicarbonate was added to the reaction mixture. Thus, adding bicarbonate did not by itself increase the amount of ethylene formed.
The competition experiments provided the most useful mechanistic clues. 2,2′-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), acting as a competing one-electron donor, strongly inhibited ethylene production. The phenolic compound 4-hydroxyphenylacetic acid also inhibited the reaction, and the combination of the two produced near-complete inhibition under the conditions examined. The patterns were similar in reactions performed with or without added bicarbonate.
Propanal (40 mM) was examined as a carbonyl surrogate for carbon dioxide in the peroxynitrite-KTBA reaction. It reduced ethylene formation by approximately 88 percent, indicating that intermediates generated in the peroxynitrite-propanal reaction were much less efficient in promoting the one-electron oxidation of KTBA.
These observations led us to favor carbonate radical as a major one-electron oxidant involved in ethylene production in these model reactions. The findings did not exclude contributions from nitrogen dioxide or other intermediates, but they were consistent with the action of a potent and comparatively selective one-electron oxidant.
Carbonate radical is generally less reactive than hydroxyl radical but more selective. That selectivity may be important in biological systems, where the most reactive oxidant is not necessarily the one that determines the observed product.
The work extended the earlier studies of Beauchamp and Fridovich and of Pryor and colleagues. It suggested that ethylene formation may arise from identifiable free-radical pathways rather than from an undefined or purely random oxidative process.
One molecule, two biological stories
To me, the central point is not simply that plants and animals produce the same molecule through different routes. It is that ethylene carries two different biological meanings.
In plants, ethylene is purposefully produced, perceived, and regulated. It coordinates ripening, growth, senescence, abscission, and responses to environmental stress. Its management also carries major agricultural and economic consequences.
In animals, the same molecule may arise as an incidental product of ongoing or episodic free-radical oxidation. Rather than functioning as a known hormone, it may provide a chemical record of oxidative activity, inflammation, or molecular injury.
Ethylene therefore represents a regulated signal in plants and a possible footprint of oxidative chemistry in animals.
This work also reflects the lasting influence of Professor William A. Pryor, whose pioneering contributions to free-radical chemistry shaped my continuing interest in oxidative biology. Parts of the experimental work were carried out in his laboratory at Louisiana State University. I also gratefully acknowledge Dr. Rafael Cueto for his indispensable assistance with GC-FID analysis.
Rao M. Uppu is professor of environmental toxicology and chemistry at Southern University and A&M College in Baton Rouge, Louisiana, where he has served since 2002. He is also an adjunct professor of chemistry and pathobiological sciences at Louisiana State University.
Trained in biochemistry, physical organic chemistry, and free radical chemistry, his research spans bioanalytical methods, biomarker discovery and validation, chemical toxicology, environmental chemistry, computational genomics, reactive intermediates, and the molecular mechanisms of disease. His scholarship is indexed on ORCID, ResearchGate, and Google Scholar.
Dr. Uppu is a Fellow of the American Association for the Advancement of Science (AAAS), the Royal Society of Chemistry (RSC), the Royal Society of Biology (RSB), the Royal Society of Medicine (RSM), the Royal Society for Public Health (RSPH), and the Academy of Toxicological Sciences (ATS).
In addition to his scientific research, he writes reflective essays on scientific culture, mentorship, peer review, ethics, and the human dimensions of academic life. He shares updates on LinkedIn.
