Person: Caito, Samuel
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Email Address
Birth Date
Biography URL
https://www.husson.edu/directory/samuel_caito
Term at University
2017-current
Research Projects
Organizational Units
Job Title
Associate Professor of Pharmaceutical Sciences
Last Name
Caito
First Name
Samuel
Name
Degrees Held
PhD Ph.D. Toxicology, 2010, University of Rochester School of Medicine and Dentistry
3 results
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Publication METHYLMERCURY ALTERATION IN THERMOGENESIS IS DIET DEPENDENT IN CAENORHABDITIS ELEGANS(2024-04-18) Varney, Abigail; Radzimirski, Anthony; Caito, SamuelThermogenesis is the process by which adipocytes metabolize triglycerides (TAG) to release energy as heat. This process is disrupted in metabolic syndrome, leading to increased TAG levels and weight gain. Methylmercury (MeHg) is an environmental toxin that has both neurotoxic and metabolic effects. We have previously shown that MeHg disrupts lipid homeostasis, leading to increased TAG content and storage sites in Caenorhabditis elegans. Furthermore, we have shown that TAG content in response to MeHg is dependent on their Escherichia coli diet. Worms fed a low lipid containing strain (HT115) showed less lipid dysregulation than worms fed a high lipid containing strain (OP50). As we have seen accumulation of TAG in response to MeHg, we hypothesized that MeHg could reduce thermogenesis in C. elegans. Worms were treated with environmentally relevant doses of MeHg, fed either OP50 or HT115, and were grown to adulthood at 15 or 25˚C. Worms were then placed at 4˚C for 48 hours and scored for survival. Untreated worms maintained at 15˚C and fed either diet were able to survive the temperature shift. MeHg significantly decreased survival of worms fed OP50 diet following the 15 to 4˚C shift, suggesting that thermoregulation was inhibited by MeHg. In contrast, MeHg had minimal effects on the survival of worms fed HT115 diet following the 15 to 4˚C shift. Shifting worms from 25 to 4˚C is lethal to all worms fed OP50. However, the HT115 diet prevented lethality in untreated or MeHg treated worms shifted from 25 to 4˚C. These data suggest that the HT115 diet is protective and can induce thermogenesis. Heat generation derives from mitochondria. HT115 fed worms had improved mitochondrial health in response to MeHg than OP50 fed worms. Taken together, our data suggests that MeHg-dependent mitochondrial damage is diet dependent leading to alterations in thermogenesis.Publication SYNERGISTIC NEUROTOXIC EFFECTS OF METHYLMERCURY AND PER-AND-POLYFLUOROALKYL SUBSTANCES (PFAS) IN CAENORHABDITIS ELEGANS(2024-04-18) Radzimirski, Anthony; Varney, Abigail; Ireland, Nicholas; Caito, SamuelMethylmercury (MeHg) is a well-known neurotoxic metal that is a major contaminant of our fish supply. Developmental exposure to MeHg causes cognitive and behavioral dysfunction in children, and cumulative exposure to MeHg has been linked to the development of neurodegenerative diseases, such as Parkinson’s disease. Recently, it has been determined that fish are becoming increasingly contaminated with per- and polyfluoroalkyl substances (PFAS). PFAS are a group of amphipathic compounds which have been used in industry for their unique property to repel both water and oils. While specific PFAS have been phased out of use and production in the United States, the environmental degradation of PFAS is slow. Both MeHg and PFAS have similar characteristics, particularly bioaccumulation and biomagnification up the food chain, ability to accumulate in the brain, and alteration in synaptic transmission of glutamate and dopamine. We therefore hypothesized that MeHg and PFAS co-exposures may synergize and produce more damage to the dopaminergic and glutamatergic nervous systems in Caenorhabditis elgans than single exposures alone. Worms were treated for 72 hours with increasing concentrations of PFOS, PFOA, or PFBS in the presence or absence of a low nontoxic dose of MeHg. Dose-response curves were generated and the lethal dose 50 (LD50) were calculated for each curve. Co-exposure of MeHg with either of the PFAS compounds shifted the dose-response curve to the left of the dose-response curve for PFAS. This suggests that the co-exposure was more toxic than PFAS exposure in worms. Glutamatergic and dopaminergic behaviors were assayed in worms treated with MeHg, PFAS, or MeHg + PFAS combination. For both behaviors, the co-exposure caused more behavioral deficits than MeHg or PFAS alone. Furthermore co-exposure to PFAS and MeHg altered both dopamine and glutamate neurotransmitter content. Taken together, our results suggest that there is a synergistic relationship between exposure to MeHg and PFAS compounds in C. elegans.Publication DELETION OF DIVALENT METAL TRANSPORTER HOMOLOGS IN Caenorhabditis elegans PREVENTS LANTHANUM- AND YTTERBIUM-INDUCED OXIDATIVE INJURY(2025-04-17) Rusiecki, Aaron; Letourneau, Lindsay; Quinlan, Alaina; Smith, Erin; Vose, Paige; Caito, SamuelLanthanide series elements are transition metals that are used in a variety of electronics, including superconductors, electronic polishers, hybrid car components, and rechargeable batteries, as well as in fertilizers, antimicrobials, contrast agents for medical imaging and diesel fuel additives. Levels of lanthanides have risen significantly in both industrial areas and environmentally. While we are starting to recognize health effects of lanthanide exposure, it is currently unknown how lanthanide metals enter cells. If we are to understand their toxicokinetics in the human body, it is imperative to determine mechanisms by which lanthanides are distributed. We hypothesized that endogenous divalent metal transporters (DMTs) are responsible for lanthanide entry into cells, and that genetic ablation of DMT transporters in Caenorhabditis elegans would protect the worms from lanthanide-induced toxicity. In this study, we treated wild type N2 or transgenic worms that lacked DMT homologs smf-1, smf-2, or smf-3, with increasing concentrations of La or ytterbium (Yb). Knock out of either of the smf genes shifted the dose-response curve for La or Yb to the right of the N2 dose-response curve, signifying protection from the mutations. We have previously observed that La and Yb cause increased body burden of oxidative stress in worms. Treatment of the smf mutant worms with La or Yb caused significantly less reactive oxygen species (ROS) generated in the worm as compared to N2 worms. Glutathione levels have been shown to decrease in N2 worms following La or Yb treatment, however GSH levels were rescued by deletion of the smf genes. Furthermore, smf mutants showed less mitochondrial damage and had increased levels of ATP as compared to N2. These results suggest that DMTs are important mediators for lanthanide series elements to enter eukaryotic cells.