Neonatal exposure to sucralose does not alter biochemical markers of neuronal development or adult behavior.
OBJECTIVE
Sucralose, a high-intensity sweetener, has been approved as a general-purpose sweetener in all food since the late 1990s. Due to its good taste and physiochemical profile, its use has increased and sucralose is considered a way of managing health and an option to improve the quality of life in the diabetic population. Recently high concentrations of sucralose have been found in the environment. Other environmental pollutants have been shown to induce neurotoxic effects when administered during a period of rapid brain growth and development. This period of rapid brain growth and development is postnatal in mice and rats, spanning the first 3-4 wk of life, reaching its peak around postnatal day 10, whereas in humans, brain growth and development is perinatal. The proteins calcium/calmodulin-dependent protein kinase II, growth-associated protein-43, synaptophysin, and tau play important roles during brain growth and development.


METHODS
In the present study, mice were orally exposed to 5-125 mg of sucralose per kilogram of body weight per day during postnatal days 8-12. Twenty-four hours after last exposure, brains were analyzed for calcium/calmodulin-dependent protein kinase II, growth-associated protein-43, synaptophysin, and tau, and at the age of 2 mo the animals were tested for spontaneous behavior.


RESULTS
The protein analysis showed no alterations in calcium/calmodulin-dependent protein kinase II, growth-associated protein-43, synaptophysin, or tau. Furthermore, there were no disturbances in adult behavior or habituation after neonatal sucralose exposure.


CONCLUSIONS
The present study shows that repeated neonatal exposure to the artificial sweetener sucralose does not result in neurotoxicity, which supports that sucralose seems to be a safe alternative for people who want or need to reduce or substitute glucose in their diet.
Viberg
Henrik
H
Department of Environmental Toxicology, Uppsala University, Sweden. Electronic address: henrik.viberg@ebc.uu.se.
Fredriksson
Anders
A
Department of Environmental Toxicology, Uppsala University, Sweden.
D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal / Q000187:drug effects* / Q000502:physiology; D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism; D004781:Environmental Exposure / Q000009:adverse effects; D019922:GAP-43 Protein / Q000378:metabolism; D006185:Habituation, Psychophysiologic / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D013395:Sucrose / Q000009:adverse effects / Q000031:analogs & derivatives*; D016708:Synaptophysin / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism
D015415:Biomarkers; D019922:GAP-43 Protein; D016708:Synaptophysin; D016875:tau Proteins; D013395:Sucrose; C026285:trichlorosucrose; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2