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DDT (dichlorodiphenyltrichloroethane) is a commonly used insecticide that is recalcitrant and highly stable in the environment. Currently, DDT residue contamination, especially in agricultural soil, is still a concern in many countries, threatening human health and the environment. Among the approaches to resolve such an issue, novel biodegradation-based methods are now preferred to physicochemical methods, due to the sustainability and the effectiveness of the former. In this study, we explored the possibility of building mixed microbial cultures that can offer improved DDT-degrading efficiencies and be more environmentally transilient, based on genome annotation using the KEGG database and prediction of interactions between single strains using the obtained metabolic maps. We then proposed 10 potential DDT-degrading mixed cultures of different strain combinations and evaluated their DDT degradation performances in liquid, semi-solid and solid media. The results demonstrated the superiority of the mixtures over the single strains in terms of degrading DDT, particularly in a semi-solid medium, with up to 40-50% more efficiency. Not only did the mixed cultures degrade DDT more efficiently, but they also adapted to broader spectra of environmental conditions. The three best DDT-degrading and transilient mixtures were selected, and it turned out that their component strains seemed to have more metabolic interactions than those in the other mixtures. Thus, our study demonstrates the effectiveness of exploiting genome-mining techniques and the use of constructed mixed cultures in improving biodegradation., (© 2024 The Author(s). Microbial Biotechnology published by John Wiley & Sons Ltd.)

Animals decrease intake of an indispensable amino acid (AA)-deficient or devoid diet, due in part to decreased dietary limiting AA (DLAA) concentrations within the anterior piriform cortex (APC), and to a recognition process that occurs as early as 20 min following exposure to AA deficiencies. Glutamate levels within the APC change in response to AA deficiencies. The APC projects to the lateral hypothalamus (LH), where glutamate acts to stimulate food intake. We hypothesize that the APC, through glutamatergic projections to the LH, inhibits the LH, which signals to reject the AA-deficient or devoid diet, and trigger aversions to the AA-deficient or devoid diet via an ascending pathway to the APC. We examined the effects of (1) bilateral APC and LH blockade of glutamate's NMDA receptors with the antagonist, D-AP5, (2) APC blockade of AMPA receptors with the antagonist, NBQX, to block glutamate transmission from the APC, and (3) direct injection of the agonist, NMDA, into the LH on intake of the AA-deficient, devoid, or corrected diet. Administration of D-AP5 into the APC increased intake of AA-deficient diet by 6 h, but D-AP5 in the LH decreased AA-devoid diet preferentially over AA corrected intake sooner. NBQX in the APC increased AA-deficient diet intake, also at 6 h. NMDA injection into the LH-stimulated intake of the AA corrected diet by 3 h, but did not affect AA-devoid diet intake. Thus, the glutamate receptors in the APC and LH are involved in the feeding responses to AA-deficient diet, albeit with regional differences. We suggest that glutamate mediates the anorectic responses to AA-deficient diets through recognition of AA-devoid diet with the glutamatergic output cells of the APC sending glutamate-based signals for changes in food intake within the LH and through learned avoidance of AA-deficient diet within the APC, as indicated through the more immediate and prolonged periods of activation within the LH and APC, respectively.

The effects of GABA(A) and GABA(B) receptors in the anterior piriform cortex (APC) on intake of an amino acid imbalanced diet and a basal diet were evaluated in rats. Administration of muscimol (GABA(A) receptor agonist) to the APC immediately suppressed ingestion of both amino acid imbalanced and basal diets. Central administration of bicuculline (a GABA(A) receptor antagonist) stimulated feeding of the amino acid imbalanced diet but had no effect on intake of the basal diet. The GABA(B) receptor antagonist phaclofen decreased consumption of the basal diet but did not affect consumption of the amino acid imbalanced diet. These findings demonstrate that manipulation of GABA-sensitive cells in the APC can have a pronounced effect on feeding behavior that is not selective to aminoprivic feeding. However, these data suggest that GABA(A) and GABA(B) receptors may function as regulators that are activated by monoaminergic systems and neuropeptides in response to amino acid imbalanced diet intake. Inhibitory effects of GABA(A) and GABA(B) receptors may modulate the pyramidal cells, contributing to the reduced feeding response to the amino acid imbalanced diet. Also, transcription of mRNA for both GABA receptors and the GABA reuptake transporter was affected by a threonine deficient but not a corrected diet, compared to the basal diet. Taken together, these results support the involvement of GABA receptors in the APC in feeding in general and the responses to amino acid deprivation in vivo.

Neuropeptides affect food intake via peripheral and brainstem mechanisms, but their roles in mediating feeding via the cerebral cortex have received little attention. The anterior piriform cortex (APC) appears to play a critical role in neuroperception of deficiencies of essential amino acids (AA) and the anorectic response to such deficiencies. The neural circuitry underlying the role of this paleocortex in these events is not understood. We have shown that neurons containing neuropeptide Y (NPY) and somatostatin (SOM) are cytoarchitecturally in positions to relate synaptically to the neurons of the APC which may mediate responses to AA. Thus, we hypothesized that NPY and SOM administered intracortically to the APC would directly affect food intake in a threonine-imbalanced model. We determined that NPY at 1-1.5 nmol decreased intake of the AA-deficient diet for 3 h, with a cumulative effect that extended through 6 h. SOM had a dual effect; at 1 pmol it increased intake of the AA-deficient diet for 3 h; at 2 nmol, SOM decreased intake of the AA-deficient diet for over 9 h, with a cumulative effect that persisted through 12 h. In the first 3 h, intake of animals receiving 1 pmol of SOM differed significantly from those receiving 2 nmol. These results suggest that NPY and SOM affect the cortical circuitry responsible for recognition of deficiencies in nutritionally essential AA, and that the timing of the cortical responses to the peptides may be related to the time course of the anorectic responses.

Repeated subthreshold stimulation of limbic brain areas increases seizure susceptibility in experimental models of epilepsy. In addition, acute dietary indispensable amino acid (IAA) deficiency activates the anterior piriform cortex (APC), a seizure-prone limbic brain area in the rat. Based on these two findings, we hypothesized that activation of the APC by chronic exposure to IAA-deficient diets might increase seizure susceptibility. Several nonessential amino acid neurotransmitters are important in seizures, but deficiencies of nontransmitter IAAs have not been well studied in seizure models. In four trials, we made injections of pentylenetetrazole intraperitoneally or of bicuculline into the APC in histidine-, isoleucine-, or threonine-deficient rats and controls. Increased susceptibility to seizures in the deficient animals was observed as increased severity of the seizures, decreased threshold for the dose of the chemostimulant and time to seizure, or a combination thereof. Pair-fed controls showed that this effect was not due to an energy deficit. This novel but robust finding suggests that IAA deficiency may increase vulnerability to seizures by repeated activation of the APC.