Curcumin, the principal active component of turmeric, is a polyphenol that has been used in various countries for the treatment of numerous conditions due to its wide range of health benefits. Curcumin exhibits bifunctional antioxidant properties: the first is attributed to its chemical structure, which enables it to directly neutralize reactive oxygen species (ROS); the second is related to its ability to induce the expression of antioxidant enzymes via the transcription factor nuclear factor erythroid 2–related factor 2 (Nrf2). Both ROS and Nrf2 are closely associated with mitochondrial function and metabolism, and their dysregulation may lead to mitochondrial dysfunction, potentially contributing to the development of various pathological conditions. Therefore, curcumin treatment appears highly promising and is strongly associated with the preservation of mitochondrial function. The aim of this review is to summarize the current literature on the impact of curcumin’s antioxidant properties on mitochondrial function. Specifically, studies conducted in different biological models are included, with emphasis on aspects such as mitochondrial respiration, antioxidant enzyme activity, interactions with mitochondrial membranes, and the role of curcumin in the regulation of intrinsic apoptosis.

Thallium (Tl) is a non-essential and highly toxic heavy metal capable of replacing potassium (K⁺) in biological systems, leading to mitochondrial dysfunction, oxidative stress, and inhibition of protein synthesis. In humans, the estimated oral lethal dose ranges from 10 to 15 mg/kg, with acute mortality rates of 6–15% and chronic neurological sequelae in up to 55% of survivors. Environmental releases of thallium of up to 5000 metric tons annually from industrial and mining activities, combined with its high oral bioavailability and nonspecific multisystemic symptoms, underscore the urgent need for more effective therapeutic strategies. This review summarizes current evidence on Tl toxicity, including its mechanisms of action, clinical manifestations, and available treatments. It emphasizes the strategic selection of biological models: simple organisms such as Caenorhabditis elegans and Drosophila melanogaster enable high-throughput screening and early biomarker detection; zebrafish (Danio rerio) provide vertebrate-level evaluation of multi-organ effects; and rodent models offer systemic toxicokinetic and therapeutic validation. Human-derived organoids and induced pluripotent stem cell (iPSC) systems recreate tissue-specific microenvironments, allowing translational assessment of mitochondrial, neuronal, and cardiac toxicity. Integrating these models within a tiered and complementary framework, alongside environmental and clinical surveillance, can accelerate the development of targeted treatments and strengthen public health responses to Tl exposure.

Vanadium is a transition metal whose environmental presence has increased due to human activities such as fossil fuel combustion and industrial processes. A central mechanism of its toxicity involves mitochondrial dysfunction, as vanadium exposure disrupts energy metabolism, enhances reactive oxygen species (ROS) generation, and triggers oxidative stress, ultimately leading to genetic damage and alterations in cellular signaling. These mitochondrial alterations contribute to its potential carcinogenic, immunotoxic, and neurotoxic properties, affecting multiple systems, including the neurological, renal, immune, and reproductive systems. Since there are no specific treatments for vanadium intoxication, natural compounds—particularly plant-derived metabolites with antioxidant, mitochondrial-targeted, and chelating properties—have been investigated as potential therapeutic agents to counteract its toxicity. In this context, simple models such as the nematode Caenorhabditis elegans (C. elegans), the fruit fly (Drosophila melanogaster), and the zebrafish (Danio rerio) have emerged as valuable experimental systems for studying vanadium-induced mitochondrial dysfunction and evaluating protective strategies. These organisms offer key advantages, including a short life cycle, ease of handling, and conservation of essential biological pathways with mammals, making them effective tools in environmental toxicology. The aim of this review is to outline the mitochondrial-related toxic effects of vanadium across different biological models and to explore plant-based therapeutic approaches capable of mitigating its harmful health impacts. We also propose the use of simple models, such as D. melanogaster, D. rerio, and, most notably, C. elegans, as versatile and complementary experimental platforms to advance research in this field.

Cadmium (Cd) is a highly toxic heavy metal that disrupts development and reproduction, primarily through oxidative stress. In this context, sulforaphane (SFN), an antioxidant compound, may serve as a promising agent to counteract Cd-induced oxidative damage and prevent developmental and reproductive abnormalities. This study aimed to evaluate the effect of SFN on reproductive toxicity induced by cadmium chloride (CdCl₂) in the nematode Caenorhabditis elegans (C. elegans). Five experimental groups were established: (I) Control: no treatment, (II) dimethyl sulfoxide (DMSO): 48 h with 0.01% DMSO, (III) CdCl₂: 24 h with 4600 µM CdCl₂, (IV) SFN + CdCl₂: 24 h with 100 µM SFN followed by 24 h with both SFN and CdCl₂, and (V) SFN: 48 h with 100 µM SFN. Co-exposure to SFN and CdCl₂ prevented the reduction in the percentage of adult nematodes and increased egg-laying. It also significantly improved hatching rates, allowing more embryos to reach the larval stage, and prevented reductions in body size. However, no effects were observed on glutathione S-transferase-4 (GST-4) levels in the transgenic CL2166 strain. In conclusion, SFN substantially prevents Cd-induced reproductive toxicity in C. elegans. Future studies should investigate the molecular mechanisms by which SFN enhances egg-laying and offspring viability in this model.

In the original publication [1], during the revisions and restructuring of the manuscript, the following references were inadvertently removed by the authors and were not cited:103