Intensified aquaculture production has significantly increased farmed fish exposure to various stressors that compromise welfare and productivity, demanding innovative approaches to enhance sustainable production. Aquaculture environments subject fish to multiple stressors. These include high-density housing, handling, transportation, and fluctuating water quality. Such stressors activate the hypothalamic–pituitary–interrenal axis, resulting in a cascade of endocrine responses. This subsequently impairs feeding behavior, growth performance, and immune function. Psychobiotics exert beneficial effects by producing neuroactive compounds, including gamma-aminobutyric acid, short-chain fatty acids, serotonin, and dopamine. Key bacterial genera such as Lactobacillus, Bifidobacterium, Bacillus, and Enterococcus demonstrate significant psychobiotic properties. Experimental evidence from zebrafish and commercially relevant species demonstrates that psychobiotic interventions consistently reduce cortisol levels, normalize stress responses, and improve behavioral outcomes. These effects occur through the microbiome–gut–brain axis, a bidirectional system connecting the nervous and gastrointestinal systems by neural, endocrine, and immune pathways. Nevertheless, significant challenges persist, such as species-specific efficacy, limitations in mechanistic understanding, and the need for standardized evaluation protocols. This review examines psychobiotics as promising interventions for stress management in aquaculture systems. We conclude that psychobiotics may offer a sustainable approach for mitigating aquaculture stress responses and enhancing both fish welfare and production efficiency through targeted microbiome modulation.

The capability of the dioxidine drug to cause bacterial resistance to antibiotics was studied. The study was performed with the use of a bioluminescent test and the recombinant E. coli strains MG 1655 (pSoxS-lux), MG1655 (pKatG-lux), MG1655 (pRecA-lux), and MG1655 (pColD-lux). The strains harbored plasmids with the operon luxCDABE from the photobacteria Photorhabdus luminescens under control of the corresponding E. coli stress-inducible promoters. The mutation frequency of the stable mutants was found by conventional methods for nonpathogenic and opportunistic strains of E. coli, Bacillus amyloliquefaciens, and Klebsiella pneumoniae. Dioxidine was shown to induce the promoters PrecA and Pcda in E. coli MG1655, which suggests the induction of the SOS-response in bacterial cells. The Pcda induction was higher than with PrecA. The value of the induction coefficient was highest if the dioxidine concentration was 2.25 × 10^–5 M. Moreover, this drug enhanced the induction of the SoxS and KatG promoters responding to the superoxide anion radical and hydrogen peroxide, which suggests possible participation of oxidative mechanisms in dioxidine DNA damage. The maximal value of the induction coefficient was also observed under conditions of 2.25 × 10^–5 M. Dioxidine can induce mutations leading to antibiotic resistance in all bacterial strains studied. An increase in mutation frequency was observed for rifampicin (twofold), ciprofloxacin (sixfold), and azithromycin (fourfold). These data show the necessity for an antibiogram for every patient who is taking or has taken dioxidine.

The use of platinum-based anticancer drugs is limited by both their side effects and their effect on normal microflora’s metagenome. Drugs that possess mutagenic and genotoxic properties may cause mutations in microbial genomes that contribute to the emergence of resistance to antimicrobial preparations and the development of complications after chemotherapy. The effects of cisplatin and oxaliplatin on microorganisms were studied using bacterial biosensors—E. coli strains MG1655 pKatG-lux, which reacts to the generation of hydrogen peroxide; MG1655 pSoxS-lux, which reacts to the superoxide anion radical; and the MG1655 pColD-lux strain, which detects DNA damage. The biosensor tests demonstrated high levels of genotoxicity for both drugs and some differences in the spectrum of reactive oxygen species generated. Ascorbate reduced genotoxicity of cisplatin by 41%. Nonlethal doses of cisplatin induced a three- to sevenfold increase in the frequency of the mutations that confer the resistance of E. coli to rifampicin and ciprofloxacin. Ascorbate also reduced frequency of the mutations by 65%. Thus, the effect of these drugs was probably associated with the generation of reactive oxygen species and induction of SOS response. The risk of secondary antibiotic-resistant infections may be decreased by applying antioxidants and antimutagens. At the same time, these increases may also decrease the anti-tumoral action of these compounds.