- General Drug Summary
- Drug Name
- Sulfadimethoxine
- Description
- Sulfadimethoxine (trade name Di-Methox, Albon) is a sulfonamide antibiotic. Sulfadimethoxine is used to treat many infections including treatment of respiratory, urinary tract, enteric, and soft tissue infections. It is most frequently used in veterinary medicine, although it is approved in some countries for use in humans. Sulfadimethoxine inhibits bacterial synthesis of folic acid (pteroylglutamic acid) from para-aminobenzoic acid.
- Also Known As
- Sulphadimethoxine
- Structure
- Summary In Neonatal Jaundice
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1 record(s) for Sulfadimethoxine Effective in Basic Research in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 22902434
- Sulfadimethoxine
- Effective in Basic Research
- Clinical Trial
- Summary
- Induce bilirubin encephalopathy
- ced neurologic dysfunction in jaundiced Gunn rat pups. Pediatric research, 2012 Nov [Go to PubMed]
- Hazardous levels of bilirubin produce oxidative stress in vitro and may play a role in the genesis of bilirubin-induced neurologic dysfunction (BIND). We hypothesized that the antioxidants taurourosdeoxycholic acid (TUDCA), 12S-hydroxy-1,12-pyrazolinominocycline (PMIN), and minocycline (MNC) inhibit oxidative stress and block BIND in hyperbilirubinemic j/j Gunn rat pups that were given sulfadimethoxine to induce bilirubin encephalopathy.
At peak postnatal hyperbilirubinemia, j/j Gunn rat pups were dosed with sulfadimethoxine to induce bilirubin encephalopathy. Pups were given TUDCA, PMIN, MNC, or vehicle pretreatment (15 min before sulfadimethoxine). After 24 h, BIND was scored by using a rating scale of neurobehavior and cerebellar tissue 4-hydroxynonenal and protein carbonyl dinitrophenyl content were determined. Nonjaundiced heterozygous N/j pups served as controls.
Administration of sulfadimethoxine induced BIND and lipid peroxidation but not protein oxidation in hyperbilirubinemic j/j pups. TUDCA, PMIN, and MNC each reduced lipid peroxidation to basal levels observed in nonjaundiced N/j controls, but only MNC prevented BIND.
These findings show that lipid peroxidation inhibition alone is not sufficient to prevent BIND. We speculate that the neuroprotective efficacy of MNC against BIND involves action(s) independent of, or in addition to, its antioxidant effects.
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1 record(s) for Sulfadimethoxine Effective in Inducing Remission in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 7478825
- Sulfadimethoxine
- Effective in Inducing Remission
- Clinical Trial
- Summary
- it displaces bilirubin from its albumin binding sites in the circulation, shifting it into tissues including the brain.
- Visual evoked potential abnormalities in jaundiced Gunn rats treated with sulfadimethoxine. Pediatric research, 1995 Aug [Go to PubMed]
- The manifestations of bilirubin encephalopathy include disturbances in the visual pathway (visual gaze paralysis and distorted visual perception). In the young jaundiced Gunn rat (jj) model of hyperbilirubinemia, significant differences in visual evoked potential (VEP) patterns have been recorded during development. In the present study, the effects of sulfadimethoxine (SDM) on VEP and electroretinogram (ERG) were examined in 3-wk-old jj rats. This drug displaces bilirubin from its albumin binding sites in the circulation, shifting it into tissues including the brain. Marked latency prolongations (11-20%) and reduced amplitudes (20-64%) were observed in the different wave components of the VEP. These changes were evident as early as 2 h after injection of the drug and persisted thereafter for another 4 h. On the other hand, ERG changes (significant prolongation of wave b) became apparent in these animals only 6 h after SDM injection. These results suggest that, although some changes in the retina may occur ater a massive entry of bilirubin into the nervous system, the primary damage in the visual pathway after bilirubin exposure is probably beyond the retina.