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No detailed data for neurotoxic effects of sodium N-chlorobenzenesulphonamide are available.

Neurotoxicity assessment is based on the similarity of chloramine B trihydrate (active substance sodium N-chlorobenzenesulphonamide trihydrate) and chloramine T (active substance tosylchloramide sodium). Upon read-across it may be assumed that chloramine B will have similar neurotoxic effects as chloramine T. Tosylchloramide sodium was used to mimic the effects of free radicals and active oxygen compounds implicated in brain ischemia and head trauma. Previous studies showed that free radicals produced both synaptic and postsynaptic damage in guinea pig hippocampal brain slices. Tosylchloramide sodium (25 to 500µM [7.0 to 140.8µg/mL]) decreased both the population spike and population postsynaptic potential. However, the ability of the population postsynaptic potential was not impaired by the treatment. These studies suggest that oxidation reactions account for the synaptic component of free radical-induced damage in the nervous system but not the postsynaptic effects. (1)

In a 90-day subchronic toxicity test all animals were observed also for neurotoxic effects. Functional observations were conducted at the end of exposure period as well as the recovery one. The sensory reactivity to auditory, visual, proprioceptive stimuli and papillary reflex was evaluated and assessment of grip strength and motor activity was conducted. No negative effects were found and Chloramine-B trihydrate was tolerated without adverse effects in male and female rats at the administered doses up to 20 mg/kg/day.

Summaries and evaluations in this section are based mostly on exhaustive and reliably peer reviewed documents: Chloramine T (CAS 127-65-1) and Metabolite p-Toluenesulphonamide (CAS 70-55-3), Review of Toxicological Literature, 2002, 16.

(1) Pellmar T.C., and K.L. Neel. 1989. Oxidative damage in the guinea pig hippocampal slice. Free Radical Biol Med 6:467-472.

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