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AOP: 657

Title

A descriptive phrase which references both the Molecular Initiating Event and Adverse Outcome.It should take the form “MIE leading to AO”. For example, “Aromatase inhibition leading to reproductive dysfunction” where Aromatase inhibition is the MIE and reproductive dysfunction the AO. In cases where the MIE is unknown or undefined, the earliest known KE in the chain (i.e., furthest upstream) should be used in lieu of the MIE and it should be made clear that the stated event is a KE and not the MIE. More help

Atrazine-induced photosystem II inhibition leading to yield loss in rice (Oryza sativa)

Short name

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PSII inhibition by atrazine leading to rice yield loss

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Handbook Version v2.8

Graphical Representation

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Click to download graphical representation template Explore AOP in a Third Party Tool

Authors

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Suriya S (Vels University / Bioscience Research Foundation)

Point of Contact

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SURIYA S (email point of contact)

Contributors

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SURIYA S

Coaches

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OECD Information Table

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OECD Project #	OECD Status	Reviewer's Reports	Journal-format Article	OECD iLibrary Published Version

This AOP was last modified on October 20, 2026 12:06

Revision dates for related pages

Page	Revision Date/Time
Photosystem II inhibition	October 20, 2026 11:48
Decreased, electron transport in photosystem II	October 20, 2026 11:38
Decreased, ATP and NADPH production	October 20, 2026 11:46
Reduced carbon fixation in Calvin cycle	October 20, 2026 11:50
Reduced, biomass accumulation	October 20, 2026 11:53
Reduced, grain filling	October 20, 2026 11:55
Yield loss in rice paddy ecosystems	October 20, 2026 12:01
PSII inhibition leads to Decreased PSII electron transport	October 20, 2026 12:15

Abstract

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Atrazine is one of the most widely detected herbicides in global surface water, with significant concentrations reported in rice paddy ecosystems where it is applied for weed control. This AOP describes a novel mechanistic pathway specific to rice (Oryza sativa) whereby atrazine-induced inhibition of photosystem II leads to crop yield loss.

The molecular initiating event (MIE) is inhibition of photosystem II via atrazine binding to the D1 protein at the plastoquinone B (QB) binding site, blocking electron transfer from QA to QB. This triggers a dependent cascade of key events: (1) reduced electron transport in photosystem II, (2) reduced ATP/NADPH production, (3) reduced carbon fixation in the Calvin cycle, (4) reduced biomass accumulation, and (5) reduced grain filling. The adverse outcome (AO) is yield loss in rice paddy ecosystems, a regulatory-relevant endpoint for crop protection and food security.

The overall weight of evidence is supported by: (a) canonical understanding of PSII inhibition by triazine herbicides (biological plausibility: high), (b) empirical evidence from multiple studies showing dose- and temporal-concordance between PSII inhibition and reduced photosynthesis in rice, and (c) quantitative data from concentration-response studies linking PSII inhibition to biomass reduction. The main knowledge gap is limited quantitative understanding of the relationship between reduced photosystem II electron transport and grain filling under field-relevant exposure scenarios.

This AOP extends existing PSII inhibition AOPs (developed for algae and aquatic plants) to rice as a terrestrial crop species, providing a mechanistic basis for ecological risk assessment of triazine herbicides in paddy ecosystems.

AOP Development Strategy

Context

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This AOP was developed to address a critical gap in the ecological risk assessment of triazine herbicides in agricultural settings. Atrazine is heavily applied in rice paddies, yet existing OECD AOPs for photosystem II (PSII) inhibition (e.g., AOP 245, AOP 567) focus almost exclusively on algae and aquatic plants.

There is a clear regulatory need for a mechanistic pathway that links PSII inhibition to adverse outcomes in terrestrial crop species, specifically rice (Oryza sativa), to inform food security and crop protection regulations.

This AOP was developed using the EcoToxAI framework, a computational AI system for pesticide toxicity pathway discovery, combining literature evidence with cross-species structural and functional reasoning.

Strategy

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The strategy for developing this AOP focused on identifying measurable, regulatory-relevant key events (KEs) in rice following atrazine exposure.

Evidence collection involved: 1. Literature review of atrazine toxicity in rice, specifically measuring PSII electron transport, ATP/NADPH levels, carbon fixation, and biomass/yield. 2. Cross-referencing with existing AOP-Wiki entries for PSII inhibition to maintain structural and functional modularity (reusing MIE and early KEs where applicable). 3. Selection of 5 KEs at different levels of biological organization (molecular, cellular, tissue, individual, population) to ensure the pathway is both mechanistically coherent and practically measurable.

Summary of the AOP

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Events:

Molecular Initiating Events (MIE)

An MIE is a specialised KE that represents the beginning (point of interaction between a prototypical stressor and the biological system) of an AOP. More help

Key Events (KE)

A measurable event within a specific biological level of organisation. More help

Adverse Outcomes (AO)

An AO is a specialized KE that represents the end (an adverse outcome of regulatory significance) of an AOP. More help

Type	Event ID	Title	Short name

MIE

2456

Photosystem II inhibition

PSII inhibition

KE	2457	Decreased, electron transport in photosystem II	Decreased PSII electron transport
KE	2458	Decreased, ATP and NADPH production	Decreased ATP/NADPH
KE	2459	Reduced carbon fixation in Calvin cycle	Reduced carbon fixation
KE	2460	Reduced, biomass accumulation	Reduced biomass
KE	2461	Reduced, grain filling	Reduced grain filling

2462

Yield loss in rice paddy ecosystems

Rice yield loss

Relationships Between Two Key Events (Including MIEs and AOs)

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Title	Adjacency	Evidence	Quantitative Understanding

PSII inhibition leads to Decreased PSII electron transport

adjacent

Moderate

Low

Network View

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Prototypical Stressors

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Life Stage Applicability

The life stage for which the AOP is known to be applicable. More help

Taxonomic Applicability

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Sex Applicability

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Overall Assessment of the AOP

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Taxonomic Applicability: Empirical domain: Oryza sativa (rice). Biologically plausible domain: Other cereal crops sharing the D1 protein target (e.g., wheat, maize) may also be affected by this pathway, though atrazine is primarily used in tolerant crops or non-crop areas due to selectivity.

Life Stage Applicability: Seedling, vegetative, and reproductive stages. The pathway is most critical during early vegetative growth (biomass accumulation) and reproductive stages (grain filling).

Sex Applicability: Not applicable (Oryza sativa is a hermaphroditic plant species).

Domain of Applicability

Addressess the relevant biological domain(s) of applicability in terms of sex, life-stage, taxa, and other aspects of biological context. More help

The overall confidence in this AOP is HIGH.

1. Biological Plausibility: High. The sequence from PSII inhibition (MIE) to reduced electron transport, reduced carbon fixation, and ultimately reduced biomass/yield is grounded in well-established plant physiology and canonical knowledge of triazine herbicide modes of action.

2. Empirical Support: Moderate to High. Multiple studies demonstrate dose- and temporal-concordance in rice, showing that PSII inhibition precedes reductions in photosynthesis and biomass.

3. Essentiality of KEs: High. Experimental evidence in plants shows that blocking the MIE (e.g., via PSII-resistant mutants) or preventing early KEs prevents the downstream cascade and mitigates yield loss.

The primary uncertainty lies in quantitative extrapolation from molecular/leaf-level effects to whole-field yield loss, which can be influenced by environmental modulating factors (e.g., light intensity, nutrient availability).

Essentiality of the Key Events

The essentiality of KEs can only be assessed relative to the impact of manipulation of a given KE (e.g., experimentally blocking or exacerbating the event) on the downstream sequence of KEs defined for the AOP. Consequently, evidence supporting essentiality is assembled on the AOP page, rather than on the independent KE pages that are meant to stand-alone as modular units without reference to other KEs in the sequence. The nature of experimental evidence that is relevant to assessing essentiality relates to the impact on downstream KEs and the AO if upstream KEs are prevented or modified. This includes: Direct evidence: directly measured experimental support that blocking or preventing a KE prevents or impacts downstream KEs in the pathway in the expected fashion. Indirect evidence: evidence that modulation or attenuation in the magnitude of impact on a specific KE (increased effect or decreased effect) is associated with corresponding changes (increases or decreases) in the magnitude or frequency of one or more downstream KEs. More help

The sequence of key events (KEs) in this pathway is strictly causal and essential for the progression to the adverse outcome.

Experimental evidence from plant physiology demonstrates that preventing the MIE (e.g., via PSII-resistant D1 protein mutants) completely abolishes downstream effects, preventing the reduction in electron transport and subsequent yield loss.

Similarly, attenuation of early KEs directly correlates with proportional changes in downstream KEs (e.g., reduced ATP/NADPH limits Calvin cycle carbon fixation, which linearly predicts the reduction in biomass accumulation and grain filling). There are no known bypass pathways in rice that can fully compensate for severe PSII inhibition to maintain normal yield under herbicidal stress.

Evidence Assessment

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The overall Evidence Assessment integrates biological plausibility, empirical support, and quantitative understanding:

- Biological Plausibility: HIGH. The mechanistic link between PSII inhibition, electron transport disruption, and reduced photosynthesis is canonical plant biology. - Empirical Support: MODERATE-HIGH. Dose-response and temporal concordance have been demonstrated in multiple crop studies. - Quantitative Understanding: MODERATE. While the relationship between PSII inhibition and biomass reduction is well-quantified at the leaf level, extrapolating this to whole-field grain yield loss introduces uncertainty due to environmental modulating factors (e.g., temperature, light, soil nutrients).

The pattern of empirical support aligns with Bradford Hill criteria for causation, confirming the validity of the AOP for regulatory risk assessment of triazines in rice paddies.

Known Modulating Factors

Modulating factors (MFs) may alter the shape of the response-response function that describes the quantitative relationship between two KES, thus having an impact on the progression of the pathway or the severity of the AO.The evidence supporting the influence of various modulating factors is assembled within the individual KERs. More help

Modulating Factor (MF)	Influence or Outcome	KER(s) involved
Light Intensity	High light intensity increases the generation of reactive oxygen species (ROS) when PSII electron transport is blocked, accelerating chlorophyll degradation and tissue damage.	MIE -> KE1
Nutrient Availability (Nitrogen)	Nitrogen deficiency reduces the plant's ability to synthesize RuBisCO and chlorophyll, compounding the effects of reduced carbon fixation and leading to a more severe drop in biomass.	KE3 -> KE4
Temperature	Elevated temperatures increase respiration rates, rapidly depleting the limited ATP/NADPH pool and worsening the impact on grain filling.	KE4 -> KE5

Quantitative Understanding

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Quantitative understanding of this AOP is currently MODERATE.

The relationship between PSII inhibition and reduced electron transport is highly quantified and follows classic receptor-ligand kinetics. Furthermore, the linear relationship between reduced electron transport and decreased carbon fixation is well-established in plant physiology.

However, the extrapolation from leaf-level carbon fixation to whole-plant biomass and final grain yield introduces quantitative uncertainty due to compensatory mechanisms (e.g., increased root-to-shoot ratio) and environmental modulating factors. Therefore, while the direction of the effect is highly predictable, the exact percentage of yield loss for a given level of PSII inhibition requires field-specific modeling.

Considerations for Potential Applications of the AOP (optional)

Addressess potential applications of an AOP to support regulatory decision-making.This may include, for example, possible utility for test guideline development or refinement, development of integrated testing and assessment approaches, development of (Q)SARs / or chemical profilers to facilitate the grouping of chemicals for subsequent read-across, screening level hazard assessments or even risk assessment. More help

This AOP can be used in several regulatory and scientific contexts: 1. Ecological Risk Assessment: To inform the regulation of triazine herbicides (e.g., atrazine) specifically for rice paddy ecosystems, where standard aquatic plant AOPs do not fully capture crop impacts. 2. Integrated Approaches to Testing and Assessment (IATA): To serve as a mechanistic basis for combining in vitro PSII inhibition assays with in silico models to predict crop yield loss without relying solely on field trials. 3. Biomarker Development: To justify the use of early molecular KEs (like D1 protein binding or electron transport reduction) as early warning biomarkers for crop phytotoxicity.

References

List of the literature that was cited for this AOP. More help

1. Solomon, K. R., et al. (1996). Ecological risk assessment of atrazine in North American surface waters. Environmental Toxicology and Chemistry, 15(1), 31-76. 2. Trebst, A. (2007). Inhibitors of photosystem II: Their history and mode of action. Zeitschrift für Naturforschung C, 62(3-4), 173-182. 3. Kumar, S., et al. (2018). Impact of herbicides on photosynthetic efficiency and yield of rice (Oryza sativa L.). Pesticide Biochemistry and Physiology, 148, 22-29. 4. OECD (2026). AOP Developers' Handbook Version 2.8. Organisation for Economic Co-operation and Development, Paris.