TY - JOUR
T1 - Memory deficits associated with sublethal cyanide poisoning relative to cyanate toxicity in rodents
AU - Kimani, S.
AU - Sinei, K.
AU - Bukachi, F.
AU - Tshala-Katumbay, D.
AU - Maitai, C.
N1 - Funding Information:
Acknowledgments Partially supported by the International Society for Neurochemistry/Committee for Aid and Education in Neurochemistry and the NIEHS and FIC grant R21ES017225 and R01ES019841 from the National Institutes of Health, Bethesda, MD.
PY - 2014/3
Y1 - 2014/3
N2 - Food (cassava) linamarin is metabolized into neurotoxicants cyanide and cyanate, metabolites of which we sought to elucidate the differential toxicity effects on memory. Young 6-8 weeks old male rats were treated intraperitoneally with either 2.5 mg/kg body weight (bw) cyanide (NaCN), or 50 mg/kg bw cyanate (NaOCN), or 1 μl/g bw saline, daily for 6 weeks. Short-term and long-term memories were assessed using a radial arm maze (RAM) testing paradigm. Toxic exposures had an influence on short-term working memory with fewer correct arm entries (F2, 19=4.57 p<0.05), higher working memory errors (WME) (F2, 19=5.09, p<0.05) and longer RAM navigation time (F 2, 19=3.91, p<0.05) for NaOCN relative to NaCN and saline treatments. The long-term working memory was significantly impaired by cyanide with fewer correct arm entries (F2, 19=7.45, p<0.01) and increased working memory errors (F2, 19=9.35 p<0.05) in NaCN relative to NaOCN or vehicle treated animals. Reference memory was not affected by either cyanide or cyanate. Our study findings provide an experimental evidence for the biological plausibility that cassava cyanogens may induce cognition deficits. Differential patterns of memory deficits may reflect the differences in toxicity mechanisms of NaOCN relative to NaCN. Cognition deficits associated with cassava cyanogenesis may reflect a dual toxicity effect of cyanide and cyanate.
AB - Food (cassava) linamarin is metabolized into neurotoxicants cyanide and cyanate, metabolites of which we sought to elucidate the differential toxicity effects on memory. Young 6-8 weeks old male rats were treated intraperitoneally with either 2.5 mg/kg body weight (bw) cyanide (NaCN), or 50 mg/kg bw cyanate (NaOCN), or 1 μl/g bw saline, daily for 6 weeks. Short-term and long-term memories were assessed using a radial arm maze (RAM) testing paradigm. Toxic exposures had an influence on short-term working memory with fewer correct arm entries (F2, 19=4.57 p<0.05), higher working memory errors (WME) (F2, 19=5.09, p<0.05) and longer RAM navigation time (F 2, 19=3.91, p<0.05) for NaOCN relative to NaCN and saline treatments. The long-term working memory was significantly impaired by cyanide with fewer correct arm entries (F2, 19=7.45, p<0.01) and increased working memory errors (F2, 19=9.35 p<0.05) in NaCN relative to NaOCN or vehicle treated animals. Reference memory was not affected by either cyanide or cyanate. Our study findings provide an experimental evidence for the biological plausibility that cassava cyanogens may induce cognition deficits. Differential patterns of memory deficits may reflect the differences in toxicity mechanisms of NaOCN relative to NaCN. Cognition deficits associated with cassava cyanogenesis may reflect a dual toxicity effect of cyanide and cyanate.
KW - Cassava
KW - Cognition
KW - Cyanate
KW - Cyanide
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U2 - 10.1007/s11011-013-9459-2
DO - 10.1007/s11011-013-9459-2
M3 - Article
C2 - 24293006
AN - SCOPUS:84895873499
SN - 0885-7490
VL - 29
SP - 105
EP - 112
JO - Metabolic brain disease
JF - Metabolic brain disease
IS - 1
ER -