## 2 Terpenoids as Semiochemicals
### Antifungal Activity  
Terpenoid compounds are often produced by plants as a defense mechanism against various pathogens, including fungi. The antifungal activity of terpenes and terpenoids might be caused by their highly lipophilic nature and low molecular weight, causing cell death or inhibiting the sporulation and germination of food spoilage fungi [34]. The capacity of disruption of the cell membrane by thymol and its closely related isomer carvacrol, by interacting with vesicles and cell membranes and through impaired ergosterol biosynthesis in Candida strains, leads to cell membrane integrity being affected by osmotic and metabolic instability and is one of the most well-known antifungal mechanisms of action [35]. Also, the synthesis of \(\beta\)-glucan and chitin, glucose polysaccharides that form the backbone of the cell wall, can be inhibited by limonene and thymoquinone, leading to damage in the fungal cell wall [36]. Mitochondrial effectiveness could be impaired by terpenes, inhibiting the action of mitochondrial dehydrogenases involved in ATP biosynthesis [35]. This inhibition can occur via the inhibition of the proton pumps in the respiratory chain, leading to a reduction in ATP production. [PERSON] et al. [37] studied the potential of a triterpenoid and tetraterpenoid in _Saccharomyces cerevisiae_ as an antifungal agent and concluded that terpenoids could play a key role in diminishing the mitochondrial content, which gives rise to an altered level of reactive oxygen species (ROS) and ATP generation. The inhibition of efflux pumps, namely, the fungal plasma membrane H\({}^{+}\)-ATPase, and their role in supporting the large transmembrane electrochemical proton gradient across the cell membrane and regulating intracellular pH, could be impaired by thymol, eugenol, and carvacrol, leading to intracellular acidification and cell death [38]. Also, a study demonstrates that terpenoids such as esucalypt D display prominent synergistic effects when used in combination with the commonly prescribed antifungal drug funconazole in resistant strains of Candida spp. via their simultaneous effect on the upregulation of the efflux pump genes CDR1 and MDR1 [39]. The inhibition of fungi nitric oxide synthase (NOS) activity may increase the effectiveness of fungicidal therapy since NO increases resistance to a broad spectrum of antifungal drugs [34]. EOs can reduce the level of nitric oxide and limit H\({}_{2}\)O\({}_{2}\) production and NO synthase, demonstrating a potential in the therapy of oxidative damage. The isoprenoid farnesol produces a toxic effect on the phytopathogenic fungus _Botrytis cinerea_, suppressing the mycelial growth and triggering apoptosis due to reactive oxygen species (ROS) accumulation [40]. Biofilms are sessile microbial and fungal communities that are strongly attached to surfaces and each other, being protected by a polymeric extracellular matrix (ECM) constituted primarily of polysaccharides. This improves their resistance against the external environment and the application of antifungal drugs and is an important virulence factor for pathogenic fungi [41]. The antibofilm activity of terpenoids is the object of new natural therapeutic alternatives, mostly derived from increasing resistance to conventional drugs,