# Application of Reproductive Toxicity Caused by Endocrine Disruptors in Rotifers: A Review

## TL;DR

This review explores how endocrine-disrupting chemicals harm rotifers, which are vital to aquatic ecosystems and aquaculture, and highlights the need for better water quality standards.

## Contribution

The study provides a comprehensive review of how different endocrine disruptors affect rotifer reproduction and identifies critical research gaps.

## Key findings

- Endocrine-disrupting chemicals reduce rotifer population density and harm offspring.
- Oxidative stress is a common mechanism of toxicity across various endocrine disruptors.
- Transgenerational effects of some chemicals weaken rotifer resilience and threaten ecosystem stability.

## Abstract

Endocrine-disrupting chemicals (substances that interfere with organisms’ hormone systems) are common in water environments and threaten ecosystems. Rotifers, key food for aquaculture larvae and important for aquatic balance, face reproductive harm from these chemicals. This study summarized how various chemicals (e.g., some plastics, heavy metals) affect rotifers’ reproduction, compared rotifer species’ sensitivity, and explored toxic mechanisms (e.g., oxidative stress, a process that causes cell damage). Results showed these chemicals reduce rotifer numbers and harm offspring. The study identifies research gaps and helps improve water quality standards, protecting aquaculture and ecosystems.

Endocrine-disrupting chemicals (EDCs), widespread in aquatic environments, interfere with endocrine function in organisms and threaten ecosystem stability. Rotifers, critical live feed for marine fish, shrimp, and crab larvae, link EDC-induced reproductive impairment to marine ecosystem stability and aquaculture sustainability. This PRISMA-compliant review synthesizes key findings, consequences, and gaps in EDC–rotifer reproductive toxicity research. Traditional EDCs (heavy metals, per- and polyfluoroalkyl substances (PFASs), phenols, phthalate esters, polybrominated diphenyl ethers (PBDEs), and steroid hormones) and emerging EDCs (disinfection byproducts, microplastics, pharmaceutical metabolites) induce distinct reproductive harm—e.g., Hg2+ shows extreme toxicity (24 h LC50 = 4.51 μg L−1 in Brachionus plicatilis), BDE-47 damages ovaries, and microplastics cause transgenerational delays. Rotifer species and exposure duration affect sensitivity (e.g., BDE-47: 96 h LC50 = 0.163 mg L−1 vs. 24 h LC50 > 22 mg L−1 in B. plicatilis). Oxidative stress is a universal mechanism, and combined EDC exposure produces context-dependent synergistic/antagonistic effects. EDC-induced impairment reduces rotifer population density, alters structure, and propagates through food webs, threatening aquaculture and biodiversity; transgenerational toxicity (e.g., 4-nonylphenol: F1 inhibition 28% vs. 12% in F0) weakens resilience. This review supports EDC risk assessment, with gaps including long-term low-concentration data, transgenerational mechanisms, EDC–microbiome interactions, and emerging PFAS toxicity—priorities for future research.