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Background Thiamine deficiency ( TD ) models have been developed, mainly using the thiamine analog pyrithiamine. Other analogs have not been used in rodents. We aimed to evaluate the effects and mechanisms of intraperitoneal (ip) amprolium‐induced TD in mice. We also evaluated the associated pathogenesis using antioxidant and anti‐inflammatory compounds (Trolox, dimethyl sulfoxide). Methods Male mice were separated into two groups, one receiving a standard diet (control animals), and the other a TD diet (deficient groups) for 20 days. Control mice were further subdivided into three groups receiving daily ip injections of saline (NaCl 0.9%; Cont group), Tolox (Tr group) or dimethyl sulfoxide ( DMSO ; Dmso group). The three TD groups received amprolium (Amp group), amprolium and Trolox (Amp+Tr group), or amprolium and DMSO (Amp+Dmso group). The animals were subjected to behavioral tests and then euthanized. The brain and viscera were analyzed. Results Amprolium exposure induced weight loss with hyporexia, reduced the behavioral parameters (locomotion, exploratory activity, and motor coordination), and induced changes in the brain (lower cortical cell viability) and liver (steatosis). Trolox co‐treatment partially improved these conditions, but to a lesser extent than DMSO . Conclusions Amprolium‐induced TD may be an interesting model, allowing the deficiency to develop more slowly and to a lesser extent. Amprolium exposure also seems to involve oxidative stress and inflammation, suggested as the main mechanisms of cell dysfunction in TD .

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Thiamine is an essential cofactor for several cellular functions. Your deficiency results in important neurological disorders, with mechanisms and lesions not fully understood. The purpose of this work was to evaluate a thiamine deficiency through the model of oral administration of amprolium in mice. The animals, treated for 20 or 80 days, received amprolium in drinking water at doses of 10, 20, and 30 mg/mL (deficient groups A, B, and C, respectively). Deficient groups A and B showed reduction in body weight gain and performance changes in the open field (decreased distance and rearing, and increased grooming) and rotarod (reduced latency to fall) behavioural tests, when treated for 80 days. However, no histological changes were observed in the central nervous system. Moreover, group B animals exposed to amprolium developed proteinuria, with moderate tubular nephrosis, at 80 days. At the highest dose (group C) there was no interest to drink water. The data suggest that the use of oral amprolium in mice may be an interesting and viable model, when using adequate exposure times and doses. The amprolium induces thiamine deficiency progressively and moderately, which may be potentially useful for disturbed pathogenesis studies.

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