On the other

hand, gastric intubation with 25 mg cypermet

On the other

hand, gastric intubation with 25 mg cypermethrin per kg bodyweight (ca. 20-40% LD50; see below for discussion) for 28 d resulted in reduced bodyweight in male Wistar rats [32]. Consumption of α-cypermethrin or curcumin alone did not affect the activities of the liver damage markers ALT, ALP, and AST in plasma in the present experiment (Table 2). The combined intake of α-cypermethrin with curcumin significantly increased plasma ALT, but not ALP or AST activities. However, because the activities of liver enzymes remained within the reference ERK inhibitor clinical trial ranges for healthy rats [26] in all groups, this statistically significant increase is likely without biological importance. In support of our

data, even high-dose feeding of 420 mg cypermethrin/kg Selleck Enzalutamide BW for 6 months did not result in increases in serum liver enzymes in rats [38]. Even the increases in the activities of liver enzymes in cypermethrin-exposed rats observed in some studies [23] and [32] remained within the reference ranges for healthy rats and are thus not indicative of hepatic injury. Hence, it appears that statistically significant effects on liver enzymes that remained within the boundaries of normal biological variation have in the past been incorrectly interpreted as pesticide-induced liver damage in some studies. α-Cypermethrin was only present in organs of animals fed the pesticide, but not of control and curcumin only-fed animals (Table 3). The fat-soluble α-cypermethrin accumulated in adipose tissues at concentrations of up to 9.8 μg/g tissue, whereas its contents

(in descending order) were much lower in kidney, liver, and brain tissues. The simultaneous ingestion of curcumin did not alter α-cypermethrin concentrations in any of these tissues (Table 3). The higher concentrations of α-cypermethrin residues in adipose compared to brain and other tissues is in agreement with observations in male Sprague-Dawley rats given a single oral dose of a mixture of four pyrethroids (each administered at 3 mg/kg bodyweight; including cypermethrin) dissolved in glycerol formal. These authors proposed that the higher concentrations and longer persistence of the pesticides in adipose tissue may be due to its slower metabolism and lack of STK38 enzymes required for pyrethroid hydrolysis [24]. Similarly, cypermethrin concentrations in rats orally administered a single dose of a mixture of six pyrethroids (of which 29% were cypermethrin) in corn oil (total pyrethroids, 27.4 mg/kg bodyweight; cypermethrin, 8 mg/kg bodyweight) were higher in adipose tissue (1.07 μg/g), than in the brain (0.14 μg/g) and liver (0.40 μg/g) 2.5 h after dosing [39]. The higher α-cypermethrin concentrations in the adipose tissues of our animals are likely explained by the longer intervention period (7 weeks vs.

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