6^th Global Summit on Toxicology and Applied Pharmacology October 17-19, 2016 (10 Plenary Forums - 1 Event)
Houston, Texas, USA

Biography:

Dr. Noreen, Toxicologist & Wellness Media Expert, also known as "The Tox Doc", is a toxicologist that specializes in environmental, space, food and nutritional toxicology. Her personal mission is to translate the language of science for non-scientists in order to educate and inform the public of critical issues that affect their health and quality of life. Dr. Noreen has completed her Doctor of Philosophy (Ph.D.), Environmental Toxicology in 2003 at the Texas Southern University. Dr. Noreen is serving as an editorial member of the Journal of Clinical Toxicology and The International Journal of Disaster Advances. Dr. Noreen has been with NASA* since 2004 & worked as the first female Space Toxicologist. She has authored a number of research articles in Space Toxicology & planetary dust toxicity.

Abstract:

Nicotine has long been regarded as one of the most toxic chemicals/drugs to human health. However, for centuries, it has also been used therapeutically.  Recently, investigations into its use for treating diseases such as ADHD, depression, Alzheimer & Parkinson diseases, digestive disorders, pain management and cognitive enhancement, have been eliciting more attention due to the development of non-prescription therapeutic products.   Given that the toxicity of over the counter (OTC) nicotine products for use in cessation of smoking is generally accepted as low-to-none, when used as directed, product developers assume that these same levels are toxicologically safe for non-smoking cessation products.  This may be the case, since the bulk of safety assessments for these products (such as electronic cigarettes) only point to risks from mishandling by non-target populations (children, pets, abusers) – not the levels of nicotine. Given the multiple routes of exposure (inhalation, ingestion and dermal absorption) that are already approved for nicotine replacement therapy (NRC) we explore and debate the best way for Toxicologists to assess non-NRC replacement therapeutic products.

Biography:

Dr. Gunnar Boysen has completed MS Biology in 1996 at the University of Kaiserslautern, The German Cancer Research Center, Heidelberg, Germany. Dr. Gunnar completed his PhD (Chemistry), Department of Chemistry University of Kaiserslautern Germany, and University of Minnesota cancer Center, Minneapolis, MN in 2002. Then in 2005 he completed Postdoctoral in the Department of Environmental Sciences and Engineering at The University of North Carolina at Chapel Hill. Dr. Gunnar Boysen is currently Associate Professor in the Department of Environmental and Occupational Health at University of Arkansas for Medical Science, USA

Abstract:

Increased glutamine uptake is known to drive cancer cell proliferation, making tumor cells glutamine-dependent. Studying lymph node aspirates containing malignant lung tumor cells showed a strong correlation between glutamine consumption and glutathione excretion. Subsequent validation in A549 and H460 lung tumor cell lines show that glutamine drives synthesis and excretion of μ molar amounts of glutathione. Glutathione is the most abundant and most widely studied endogenous antioxidant. Glutathione concentrations in normal tissues are in the µmolar range, which is 10,000 fold higher than the concentration of reactive oxygen species. This stoichiometric disconnect has been poorly understood. To understand the molecular function of μ molar concentrations of glutathione in lung tumor model we studied glutathione metabolism. Glutathione is degraded by γ-glutamyl transpeptidase (GGT) by transferring the glutamyl group to amino acids to facilitate the amino acid uptake. Inhibition of glutaminase or GGT essentially abolished glutathione synthesis and formation of γ-glutamyl amino acids. Both enzymes were found to be essential for cell proliferation. Quantitative evaluation of glutathione’s many functions led us to believe that glutathione’s main function is to store building blocks for biosynthesis and trigger cell proliferation or apoptosis, depending on nutrition availability. Consequently, cell viability is mainly controlled by a stable metabolite, glutathione, instead of the common belief that these processes are controlled by unstable radical chemistry.

Biography:

Bangyan Stiles joined the faculty of the Department of Pharmaceutical Sciences to form the Department of Pharmacology and Pharmaceutical Sciences, at the USC School of Pharmacy in December 2005. She was promoted to Associate Professor with tenure in 2012. Over the past ten years, she has built a successful program that allows her team to explore the complicated pathogenesis of chronic disease and apply therapies to test the translational value of our discoveries. Her group is the leader in understanding the contribution of lipid metabolism to liver cancer targeting the phosphatidylinositol-3 kinase (PI3K) and related signaling pathway.

Abstract:

Liver kinase B 1 (LKB1 or STK11) and PTEN (phosphatase and tensin homologue deleted on chromosome 10) are two tumor suppressors that both regulate the mTOR signaling pathway. Deletion studies show that loss of either Stk11 or Pten leads to liver injury. In this study, we investigated the molecular mechanisms underlying such toxicity. We show here that the hepatocyte transporter for bilirubin, multidrug resistant protein (MRP2) is significantly affected by LKB1 loss, correlating with the increases in plasma bilirubin levels. Both the levels and localization of MRP2 are altered by LKB1 loss. MRP2 levels are significantly reduced as a result of LKB1 loss in the liver of Stk11 (LKO) or Stk11/Pten (LPKO) double deleted mice vs. the controls. MRP2 is a multi-drug resistant transporter localized to the canalicular membrane of hepatocytes in the control. MRP2 functions to transport various molecules across the apical membrane including bilirubin. In the LKO and LPKO livers, the canalicular localization of MRP2 is lost and became diffusely localized to both nucleus and the cytoplasm. This observed regulation of MRP2 by LKB1 likely contributed to the lack of cellular polarity and the early lethality phenotype associated with LKO mice.

Biography:

Luis A Lopez-Fernandez is currently the Head of the Laboratory of Pharmacogenetics and Pharmacogenomics at Hospital General Universitario Gregorio Marañón in Madrid, Spain. He has completed his PhD from the University of Alcalá de Henares and Post-doctoral studies from Spanish Research Council and Centre de Biochimie (Nice, France). He is a Member of the Board of the Spanish Society of Pharmacogenetics and Pharmacogenomics. He was granted a Miguel Servet II position for young researchers. He has published more than fifty articles in international journals in the fields of oncology, genomics and pharmacogenetics.

Abstract:

Adverse reactions (ADRs) to chemotherapy agents, which can lead to treatment discontinuations and to the loss of treatment lines, are one of the major issues in the treatment of colorectal cancer. Individual genetic variants affect susceptibility to these adverse reactions. Several polymorphisms have been identified although they still need validation due to controversial results. Furthermore, new genetic variants need to be identified to increase the prediction power of existing tests. The aim of our work is to validate previously identified polymorphisms and to identify new variants. Three different approaches were followed: an association study of previously identified SNPs with adverse reactions to capecitabine-based treatments in a cohort of colorectal cancer patients, an association study of tag-SNPs with adverse reactions to capecitabine-based treatments in the same cohort, and a whole exome study in eight colorectal cancer patients suffering from high toxicity to capecitabine-based treatments. Results validate several SNPs associated with ADR to capecitabine in CRC. A test can identify patients at high risk of severe overall toxicity more precisely than regular tests. Tag-SNPs allow identifying new SNPs related to ADR in fluoropyrimidine-treated patients. Finally, exome sequencing allows us to obtain a complete profile of genetic variants in exons, splice sites and 5’ and 3’ untranslated regions in all genes participating in fluoropyrimidine pathway. In summary, this global approach is an excellent way to increase the knowledge of fluoropyrimidine-related adverse reaction pharmacogenetics and to increase the predictive power of pharmacogenetic tests in this field.

Biography:

G. Jean Harry, Ph.D., is head of the Neurotoxicology Group. She obtained an M.S. in neuropharmacology from Virginia Commonwealth University with a research focus in drugs of abuse. Her Ph.D. was obtained from VCU in 1981, and bridged the fields of neuropharmacology and neurotoxicology with her research conducted at NIH. Postdoctoral work was conducted in an NIH Training Program in Neuropathology followed by an NIH independent fellowship award in the Biochemistry Department, University of North Carolina. Following a position within the Developmental Disorders Center at UNC, she joined NIEHS as head of Neurotoxicology Group in 1990.

Abstract:

Neuroinflammation is associated with a variety of states within the brain including injury, disease, neurological disorders, and aging.  These states have often been associated with a morphological shift in the brain monocyte, the microglia, suggesting an anatomical approach to determining the neuro-inflammatory responses. Of concern is the heterogeneity of the microglia response and the beneficial versus detrimental nature of the response and how this relates to morphological changes in microglia is not clearly characterized. As the primary cellular source for inflammatory factors, microglia serve surveillance, maintenance and repair functions and display varied phenotypes, some beneficial while others require active regulatory control. Dissecting the distinct phenotypes of microglia subsets as associated with various functions (e.g., clearance of debris, synaptic remodeling and neuronal protection) is a critical step in characterizing unique responses contributing to functional differences. Using the trimethyltin mouse model of inflammatory-related hippocampal injury, resident microglia morphological heterogeneity was examined across hippocampal sub-regions and found to be associated with a spatial and temporal elevation of pro and anti-inflammatory cytokines, iNos, and complement expression. These patterns were differentially associated with neuronal death and synaptic loss but were also related to the repair mechanisms initiated.  Upon further examination by protein micro-characterization, unique profiles were demonstrated in the distinct hippocampal regions suggestive of phenotypic classifications of microglial and their environmental niches. Further examination of microglia heterogeneity of morphology and associated molecular/biochemical factors will significantly contribute to our understanding of the functional impact of a microglia/neuroinflammatory response following chemical exposure.

Biography:

Chunxu Hai is Professor from Fourth Military Medical University. He is the Director of Shaanxi Key Lab of Free Radical Biology and Medicine, Fourth Military Medical University. As corresponding author, he has published more than 40 SCI-indexed papers in reputed journals and has been serving as an Editorial Board Member of repute.

Abstract:

The present study was designed to investigate the effect of diosgenin (DSG) on metabolic dysfunction and to elucidate the possible molecular mechanisms. High fat (HF) diet-fed mice and 3T3-L1 preadipocytes was used to evaluate the effect of DSG. We showed that DSG attenuated metabolic dysfunction in HF diet-fed mice, as evidenced by reduction of blood glucose level and improvement of glucose and insulin intolerance. DSG ameliorated oxidative stress, reduced body weight, fat pads, and systematic lipid profiles and attenuated lipid accumulation. DSG inhibited 3T3-L1 adipocyte differentiation and reduced adipocyte size through regulating key factors. DSG inhibited PPARγ and its target gene expression both in differentiated 3T3-L1 adipocytes and fat tissues in HF diet-fed mice. Overexpression of PPARγ suppressed DSG-inhibited adipocyte differentiation. DSG significantly increased nuclear expression of ERβ. Inhibition of ERβ significantly suppressed DSG-exerted suppression of adipocyte differentiation and PPARγ expression. In response to DSG stimulation, ERβ bound with RXRα and dissociated RXRα from PPARγ, leading to the reduction of transcriptional activity of PPARγ. These data provide new insight into the mechanisms underlying the inhibitory effect of DSG on adipocyte differentiation and demonstrate that ERβ-exerted regulation of PPARγ expression and activity is critical for DSG-inhibited adipocyte differentiation.

Biography:

Carlos Horacio Laino received his PhD degree in Pharmacology from University of Buenos Aires, Argentina and completed his Post-graduate studies in the laboratory of the Research Department of Neuroscience, Center for Addiction and Mental Health, Research Foundation of Toronto, Canada. Then, he joined the National University of La Rioja (Argentina) in 2005 and is currently an Associate Professor of Pharmacology and Toxicology. He further received an award for Innovative Research Work from the National Innovation Submit & Showcase Tech Connect World in 2013 and 2014. His research focuses on drug discovery in several therapeutic areas, especially pain.

Abstract:

The treatment of acute and chronic severe pain remains a major daily challenge for health professionals in clinical practice. Chronic pain impairs the quality of life, especially of the elderly. With the increase in life expectancy, the development of chronic pain secondary to degenerative diseases or various types of cancer has also increased. Morphine is a potent analgesic mostly used to control pain. However, long term treatment develops several problems, such as loss of analgesic efficacy (tolerance), increased sensitivity to pain (hyperalgesia) and adverse effects like constipation, nausea, vomiting, sedation, drowsiness, pruritus and weight loss. These effects, together with tolerance and hyperalgesia, may require the use of increasingly higher doses to get the same analgesic effect or discontinue its use, which constitutes a failure of the treatment against pain. Also, because morphine has a short analgesic effect, doses should be administered every 4 hours, causing difficulties for the patient. This project describes a technological development with an innovative character, both in its pharmaceutical composition (morphine and omega-3 fatty acids) and in the pharmacological treatment associated with its use. The main advantage of the new pharmaceutical composition and pharmacological treatment lies in the control of pain with a sub-therapeutic dose of morphine which would eliminate or potentially decrease its adverse effects. Other important clinical benefits of using it in terminally ill patients, (such as cancer sufferers) or patients with other types of chronic diseases are the decrease in tolerance to analgesic effect and the reduction in body weight loss and constipation.

Biography:

Xue Zhou received her BS degree in Environmental Sciences from Wuhan University in 2003 and obtained her PhD degree in Environmental Health Sciences from New York University in 2010. She is currently Associate Professor at School of Public Health, Huazhong University of Science and Technology. She has more than 20 publications in reputed journals.

Abstract:

Organically modified rectorite (OREC) micro/nanoparticles can be synthesized by organic modification from calcium rectorite (Ca²⁺-REC or REC), a common form of rectorite in nature. Although REC and OREC have potential applications in food packing and drug delivery, their cytotoxicity is not clear. In the present study, we investigated and compared the cytotoxicity of REC and OREC micro/nanoparticles in Chang liver and HepG2 cells. The interlayer spacing of OREC was enlarged after organic modification. REC and OREC could be taken up by Chang liver cells after treatment. REC and OREC induced cytotoxicity in Chang liver and HepG2 cells at almost all doses (1, 2.5, 5, 7.5, and 10μg/mL) after 6, 24, and 48 h of treatment (P<0.05 or P<0.01). OREC was more cytotoxic than REC. However, there was no difference in the cytotoxicity of REC and OREC between the two cell lines. After treatment with REC or OREC at 7.5 and 10μg/mL for 24 h, the apoptotic and necrotic percentages of Chang liver cells were increased (P<0.05 or P<0.01). The levels of apoptosis-related proteins Bax, Bcl-2, and pro-caspase-3 were all decreased in Chang liver cells after 24h of exposure to REC or OREC at 5, 7.5 and 10μg/mL. There was no change in Bax/Bcl-2 ratio after treatment, indicating that REC or OREC-induced apoptosis was not associated with Bax-related mitochondria-mediated apoptotic pathway. Our results suggested that OREC was more cytotoxic than REC, but the underlying mechanisms need further investigation.

Biography:

Xin Wang has completed his PhD from Fourth Military Medical University. He is the Vice Director of Department of Toxicology, Fourth Military Medical University. As first author or corresponding author, he has published 20 SCI-indexed papers in reputed journals and has been serving as an Editorial Board Member of several journals.

Abstract:

In view of the critical role of redox system in numerous physiological and pathophysiological processes, it is important to clearly understand the constitution and regulatory mechanism of redox system. In this work, we will systematically review the current data detailing the reactive oxygen species (ROS), enzymatic and non-enzymatic antioxidants and redox sensitive transcription factors and we give a brief description of redox-exerted epigenetic and post-translational regulation. We propose that the redox system functions as a “Redox Chain”, consisting of “ROS-generating Enzyme Chain”, “Combined Antioxidant Chain” and “Transcription Factor Chain”. We suggest that redoxomic techniques should be extensively applied to understand the biological effects of redox alterations in a more integrated way. A stable and standardized “redox index” is urgently needed for the evaluation of the general redox status. We suggest that for the redox intervention of an individual, an individualized assessment of the redox status in the body should be conducted. The strategy of intervention is to maintain general redox balance rather than to conduct simple pro-oxidant or anti-oxidative interventions. These findings provide valuable new insights into redox system and open up new paths for the control of redox-related disorders.

Biography:

Arunava Ghosh completed his Bachelor of Science degree in Zoology and Master of Science degree in Environmental Science from Calcutta University. He has completed his PhD from Calcutta University in Biotechnology in 2013. In his Doctoral research, he investigated the effects of smoke exposure on protein modification and emphysematous lung damage. At present he is carrying out Post-doctoral studies in Dr. Robert Tarran’s lab at Marsico Lung Institute/UNC CF Center, University of North Carolina at Chapel Hill as Postdoctoral Research Associate (TCORS School of Medicine). His present research endeavors are focused on the effects of New and Emerging Tobacco Products on lung.

Abstract:

Cigarette smoking has been identified as the most important source of morbidity and mortality worldwide. Generally the life expectancy of smokers is nearly 14 years less than nonsmokers Apart from causing the various life-threatening diseases, cigarette smoke (CS) is also known to produce hypoxia.  Chronic hypoxia may be a cause of early aging, morbidity and premature death. Also, smoking during pregnancy causes reduced availability of oxygenated blood to the fetus resulting in intrauterine hypoxia and various risks for the unborn child.  Earlier we had shown that p-benzoquinone (p-BQ), derived from p-benzosemiquinone of CS in the smoker’s lungs, gets into the blood stream and forms covalent adducts with serum albumin resulting in alteration of its structure and ligand binding capacity. Here we show by mass spectrometric analyses that in smoker’s blood p-BQ forms covalent adducts with cysteine 93 residues in both the β chains of hemoglobin (Hb) producing Hb-p-BQ adducts. UV-Vis spectra and CD spectra analyses show that upon complexation with p-BQ, the structure of Hb is altered.  Compared to nonsmoker’s Hb, the content of α-helix decreased significantly in smoker’s Hb (p=0.0224). p-BQ also induces aggregation of smoker’s Hb as demonstrated by SDS-PAGE, dynamic light scattering and atomic force microscopy. Alteration of Hb structure in smoker’s blood is accompanied by loss of oxygen binding capacity. Our results provide the first proof that p-BQ is a cause of hypoxia in smokers.

Biography:

Danila Cuomo is a PhD student in Science for Environment and Health at University of Sannio in Italy. She is performing her research activity in the Prof. Ambrosino Systems Toxicology Laboratory at Biogem in Ariano Irpino. In spring 2015, she was a research scholar at Health Science Center of Texas A&M University in College Station, TX. Her work aims to investigate the impact of environmental issues on endocrine system. Recently, she is focusing on reproductive health. Using OMICS approaches, she aspires to identify novel biomarkers detectable in human fluids, useful to predict reproductive diseases, such as premature ovarian aging.

Abstract:

Toxicogenomics accomplished to standard toxicology are considered a powerful method for low-dose endocrine disruptor compounds (EDCs) testing. In recent years, it has been developed a strong demand for reducing the use of small mammals in chemical testing. To meet this need, it is necessary to estimate the possibility of validly replacing them with cellular and no-mammal models. We explored this aspect investigating the activity of BPA as EDC in immortalized rat follicular cell line (FRTL-5), in primary pancreatic islets and hepatocytes, models for endodermal cells. In FRTL-5 environmental doses of BPA induce the transcription of thyroid specific genes and their transcriptional regulators. Furthermore, we highlighted the activation of NF-kB pathway in thyrocytes after BPA exposure. Basic on our data, we developed a reporter cell line able to sense BPA at very low concentrations. By gene expression analysis, we revealed that thyrocyte transcriptome reacts dynamically to low-dose BPA exposure. Particularly, we uncovered its capability to weaken cellular response to a further stress factor. Environmental exposure to BPA does not impact hepatocyte transcriptome. On the other side, the expression of few genes is altered in ex-vivo cultured pancreatic islets, leading to impairment of mitochondrial activity and apoptosis. Also in this case, the experimental activity highlighted that BPA exposure can alter cells ability to respond to damages. Overall, we propose new mechanisms for BPA toxicity that are exerted, exclusively, in presence of further stressors. This observation suggests revisions in the development of experimental plans including multiple exposure conditions.

Biography:

Ahmad Sharanek has obtained a Master’s degree in Cancerology from the Lebanese University in Beirut. He traveled to France to prepare a PhD on mechanisms of drug-induced liver injuries under the supervision of Professor André Guillouzo. He obtained his PhD in June 2015 from Rennes 1 University and is currently pursuing Post-doctoral studies at Rennes 1 University. He has published 6 papers in reputed journals.

Abstract:

Intra-hepatic cholestasis is a frequent manifestation of drug-induced liver injury in humans and its prediction represents a major challenge. We aimed to investigate mechanisms involved in drug-induced cholestasis using human HepaRG cells. We found that bile canaliculi (BC) of untreated HepaRG hepatocytes underwent spontaneous contractions, which are essential for bile acid (BA) efflux and require alternations in myosin light chain phosphorylation/dephosphorylation. Short-term treatment with prototypical cholestatic compounds was found to result in alterations of BC dynamics typified by either constriction or dilation of BC. These morphological alterations were associated with disruption of the ROCK/MLCK/myosin pathway either directly or by targeting different levels of the ROCK/MLCK axis and its associated MAP-kinases. HepaRG cells produced normal conjugated BAs. Cholestatic drugs showed variable potency to cause BAs accumulation: different total BAs content and BAs profiles in either supernatants or cell layers were evidenced. Repeated treatments as well as co-treatments with pro-inflammatory cytokines, IL1 and IL6, aggravate cholestatic features induced by certain cholestatic drugs. Together, these results provide the first demonstration that cholestatic drugs alter BC structures by targeting the ROCK/MLCK pathway and cause BAs accumulation concomitantly to occurrence of various other cholestatic features, in an in vitro human liver cell model, thereby mimicking drug-induced in vivo liver cholestasis. These studies highlight new insights into mechanisms underlying bile flow failure and can be used to identify new predictive biomarkers and therapeutics of drug-induced cholestasis

Biography:

Alicja Urbaniak received her MSc degree in Chemistry at the Adam Mickiewicz University in Poznan, Poland, where she continued her chemistry education as a PhD student. Since June 2016, she has worked as a graduate student at University of Arkansas for Medical Sciences in Prof. Anna Radominska-Pandya’s group. She was awarded the best Master’s Thesis in quantum chemistry when she defended in Poland in 2012. She is an author of four scientific papers and presented her research results at 32 scientific conferences. Her scientific interests are related to the organic chemistry of natural compounds and their metabolism.

Abstract:

Resveratrol (3, 5, 4`-trihydroxy-trans-stilbene, tRV) is a polyphenol found in numerous plant species, e. g. grapes, berries, peanuts, that exhibits many beneficial properties namely antioxidant, anti-inflammatory and cytostatic. However, its wide application is limited due to its rapid metabolism and low solubility. Our laboratory synthesized 16 derivatives of tRV by conjugation with other bioactive compounds such as hydroxycinnamic acids. Rigorous structure identification was carried out, and the crystal structure of selected compounds was determined. In this work, tRV esters were tested for biological activity. Specifically, radical scavenging effect, elastase, collagenase and the inhibitory activity of tyrosynase and cholinesterases were investigated in vitro studies. Interestingly, resveratryl tri-p- and tri-m-coumatare were the best inhibitors of both cholinesterases. We have also checked the ability of resveratrol esters to bind to and activate CB1 and CB2 cannabinoid receptors. Preliminary data indicates that several of tRV esters also bind to CB1 and CB2 with low affinity (µmol range) but comparable to tRV. Based on these observations, we hypothesiezed that CB1 and CB2 receptors may play an important role in the molecular mechanism of action for tRV esters. Minor modifications to the basic tRV structure resulted in marked alterations in the affinity of various analogs for CBRs; this indicates that tRV could be used as a scaffold for the design of highly selective and efficacious CB1R and CB2R ligands. It is expected that the conjugation of tRV with other bioactive compounds may lead to synergistic biological effects and, consequently, higher activity as compared to the unbound, individual components.

Biography:

Abstract:

Aflatoxin B₁ (AFB₁) is a class 1 carcinogen and a common food contaminant worldwide. It is also a major cause of the development of hepatocellular carcinoma (HCC), making dietary exposure to this toxin very concerning. Existing strategies to reduce AFB₁ exposure are limited and as a result, many people are exposed to this toxin worldwide. Issues with current detoxification strategies include harmful byproduct formation, incomplete removal, or the requirement of sophisticated infrastructures. Our study aims to develop a new chemical treatment process to modify AFB₁ into a non-carcinogenic form using benign reagents found in human diets. Our strategy targets the mutagenic site of the AFB₁ molecule, the 8,9-double bond, by adducting it to selected amino acids in dietary proteins. Identification and quantification of aflatoxins was performed using high performance liquid chromatography-electrospray ionization-time of flight mass spectrometry (HPLC-ESI-TOFMS). Optimization of AFB₁ hydration was carried out by incubating in various organic acids as well as increasing temperature. Newly formed AFB_2a was introduced to alkaline solutions containing amino acids, peptides, and other biological molecules. Products were identified based on changes in retention times and accurate mass values. Mutagenicity of the resulting adduct was determined using an Ames’ test with and without the presence of hepatic microsomes. This study provides a basis for developing a safe and effective detoxification method for contaminated foods, reducing exposure to AFB₁ worldwide.