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Piao FY, Xie XK, Yamamoto H, et al. Effect of phenylmethylsulfonyl fluoride administration prior to and following leptophos administration on electrolyte concentration and enzyme activity in hen serum. Environ Health Prev Med. 1996;1(1):44-50doi: 10.1007/BF02931172.
Piao, F. Y., Xie, X. K., Yamamoto, H., & Kitabatake, M. (1996). Effect of phenylmethylsulfonyl fluoride administration prior to and following leptophos administration on electrolyte concentration and enzyme activity in hen serum. Environmental health and preventive medicine, 1(1), 44-50. https://doi.org/10.1007/BF02931172
Piao, F Y, et al. "Effect of phenylmethylsulfonyl fluoride administration prior to and following leptophos administration on electrolyte concentration and enzyme activity in hen serum." Environmental health and preventive medicine vol. 1,1 (1996): 44-50. doi: https://doi.org/10.1007/BF02931172
Piao FY, Xie XK, Yamamoto H, Kitabatake M. Effect of phenylmethylsulfonyl fluoride administration prior to and following leptophos administration on electrolyte concentration and enzyme activity in hen serum. Environ Health Prev Med. 1996 Apr;1(1):44-50. doi: 10.1007/BF02931172. PMID: 21432420.
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Environ Health Prev Med. 1996 Apr;1(1):44-50. doi: 10.1007/BF02931172.

Effect of phenylmethylsulfonyl fluoride administration prior to and following leptophos administration on electrolyte concentration and enzyme activity in hen serum.

Environmental health and preventive medicine

F Y Piao, X K Xie, H Yamamoto, M Kitabatake

Affiliations

  1. Department of Public Health, School of Medicine, Mie University, 2-174 Edobashi, 514, Tsu, Mie-Pref, Japan.

PMID: 21432420 DOI: 10.1007/BF02931172

Abstract

We observed acute toxicity, delayed neurotoxicity, disappearance of leptophos from tisuues and biochemical changes in four groups of hens: a group given only 30 mg/kg leptophos (iv) as the 'leptophos group', two groups given a treatment of 30 mg/kg phenylmethylsulfonyl fluoride (PMSF) (sc) 24 hr prior to (as the 'pretreated group') and following (as the 'posttreated group') administration of the same dose of leptophos as the leptophos group, and a group given a vehicle only as the 'control group'. All groups other than the control group showed acute toxicity. The scores for organophosphate-induced delayed neurotoxicity (OPIDN) in the posttreated group reached the maximal level on the 16th day after leptophos administration and those in the leptophos group reached the maximal level on the 25th day. Serum acid phosphatase (AcP) activities in the leptophos group and the posttreated group were significantly lower than that in the control group (p<0.05) on the 6th day after leptophos administration and then recovered to the normal level on the 15th day. In these two groups, serum creatine phosphokinase (CPK) activity was significantly higher (p<0.01) and the concentration of serum Ca(2+) was significantly lower (p<0.05) than in the control group on the 15th day after leptophos administration. Serum leucine aminopeptidase (LAP) activity in the posttreated group was significantly lower than that in the control group (p<0.01). As for the significant changes by time interval between the 6th and the 15th days after leptophos administration, CPK activity was elevated and serum Ca(2+) reduced in both the leptophos group and the posttreated group, and LAP activity was also reduced in the posttreated group. The courses of leptophos disappearance in several tissues of these hens were similar in the 3 groups. These results suggest that the treatment by PMSF prior to or following the administration of leptophos can significantly modify not only clinical signs of OPIDN but also changes of several biochemical indices accompanied by OPIDN. Furthermore, it is possible to expect that these biochemical indices can provide some valuable clues for exploring the modification of OPIDN by PMSF treatment.

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