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Abstract：
UNASSIGNED: The study was carried out to assess the effect of zinc supplementation on changes in calcium homeostasis, and parathyroid gland, bone, and skeletal muscle histology in rats exposed to subchronic oral glyphosate-based herbicide (GBH, GOBARA®) toxicity.
UNASSIGNED: Sixty male Wistar rats in 6 equal groups (DW, Z, G1, G2, ZG1, ZG2) were used: DW and Z were given 2 mL/kg distilled water and 50 mg/kg of zinc chloride (2%), respectively; G1 and G2 received 187.5 mg/kg and 375 mg/kg of glyphosate (in GBH), respectively; ZG1 and ZG2 were pretreated with 50 mg/kg of zinc chloride before receiving glyphosate, 1 hour later, at 187.5 and 375 mg/kg, respectively. Treatments were by gavage once daily for 16 weeks. Serum calcium, vitamin D, and parathormone were estimated. Histopathological examination of parathyroid gland, femoral bone and biceps femoris muscle was done.
UNASSIGNED: GBH exposure caused significant (P = .0038) decrease in serum calcium concentration in G1, significant (P = .0337) decrease in serum vitamin D concentration in G1, significant increases in parathormone in G1 (P = .0168) and G2 (P = .0079) compared to DW. Significant (P > .05) changes did not occur in the other parameters of G2 compared to DW. Dose-dependent effect in GBH exposure was not observed after comparing G1 and G2. Necrotic changes occurred in parathyroid gland cells, osteocytes, and muscle cells in G1 and G2. In ZG1 and ZG2, significant (P > .05) variations in the parameters were not observed and tissue lesions were absent.
UNASSIGNED: Subchronic GBH exposure impaired calcium homeostasis observed as hypocalcemia, hypovitaminemia D, and secondary hyperparathyroidism and caused tissue damage in parathyroid gland, bone, and muscle of rats and these were mitigated by zinc chloride pretreatment.
UNASSIGNED: Sixty male Wistar rats in 6 equal groups (DW, Z, G1, G2, ZG1, ZG2) were used: DW and Z were given 2 mL/kg distilled water and 50 mg/kg of zinc chloride (2%), respectively; G1 and G2 received 187.5 mg/kg and 375 mg/kg of glyphosate (in GBH), respectively; ZG1 and ZG2 were pretreated with 50 mg/kg of zinc chloride before receiving glyphosate, 1 hour later, at 187.5 and 375 mg/kg, respectively. Treatments were by gavage once daily for 16 weeks. Serum calcium, vitamin D, and parathormone were estimated. Histopathological examination of parathyroid gland, femoral bone and biceps femoris muscle was done.
UNASSIGNED: GBH exposure caused significant (P = .0038) decrease in serum calcium concentration in G1, significant (P = .0337) decrease in serum vitamin D concentration in G1, significant increases in parathormone in G1 (P = .0168) and G2 (P = .0079) compared to DW. Significant (P > .05) changes did not occur in the other parameters of G2 compared to DW. Dose-dependent effect in GBH exposure was not observed after comparing G1 and G2. Necrotic changes occurred in parathyroid gland cells, osteocytes, and muscle cells in G1 and G2. In ZG1 and ZG2, significant (P > .05) variations in the parameters were not observed and tissue lesions were absent.
UNASSIGNED: Subchronic GBH exposure impaired calcium homeostasis observed as hypocalcemia, hypovitaminemia D, and secondary hyperparathyroidism and caused tissue damage in parathyroid gland, bone, and muscle of rats and these were mitigated by zinc chloride pretreatment.
摘要：
■这项研究是为了评估补锌对钙稳态变化的影响，和甲状旁腺,骨头,和暴露于亚慢性口服草甘膦除草剂的大鼠的骨骼肌组织学(GBH，GOBARA®)毒性。
■60只雄性Wistar大鼠，分为6组（DW，Z,使用G1，G2，ZG1，ZG2）：DW和Z分别给予2mL/kg蒸馏水和50mg/kg氯化锌（2％），G1和G2分别接受187.5mg/kg和375mg/kg的草甘膦（在GBH中），ZG1和ZG2在接受草甘膦前分别用50mg/kg氯化锌预处理，1小时后,在187.5和375毫克/千克，分别。治疗通过每天一次管饲法进行,持续16周。血清钙，维生素D,和甲状旁腺激素估计。甲状旁腺的组织病理学检查，进行股骨和股二头肌。
■GBH暴露导致G1期血清钙浓度显着降低（P=.0038），G1期血清维生素D浓度显着降低（P=.0337），与DW相比，G1期（P=.0168）和G2期（P=.0079）的副激素显着增加。与DW相比，G2的其他参数没有发生显着变化（P>0.05）。比较G1和G2后，未观察到GBH暴露的剂量依赖性效应。坏死性改变发生在甲状旁腺细胞，骨细胞,和肌肉细胞在G1和G2。在ZG1和ZG2中，未观察到参数的显着变化（P>.05），并且没有组织病变。
■亚慢性GBH暴露损害钙稳态，观察到低钙血症，低维生素D,和继发性甲状旁腺功能亢进，引起甲状旁腺组织损伤，骨头,和大鼠的肌肉，这些被氯化锌预处理减轻。
■60只雄性Wistar大鼠，分为6组（DW，Z,使用G1，G2，ZG1，ZG2）：DW和Z分别给予2mL/kg蒸馏水和50mg/kg氯化锌（2％），G1和G2分别接受187.5mg/kg和375mg/kg的草甘膦（在GBH中），ZG1和ZG2在接受草甘膦前分别用50mg/kg氯化锌预处理，1小时后,在187.5和375毫克/千克，分别。治疗通过每天一次管饲法进行,持续16周。血清钙，维生素D,和甲状旁腺激素估计。甲状旁腺的组织病理学检查，进行股骨和股二头肌。
■GBH暴露导致G1期血清钙浓度显着降低（P=.0038），G1期血清维生素D浓度显着降低（P=.0337），与DW相比，G1期（P=.0168）和G2期（P=.0079）的副激素显着增加。与DW相比，G2的其他参数没有发生显着变化（P>0.05）。比较G1和G2后，未观察到GBH暴露的剂量依赖性效应。坏死性改变发生在甲状旁腺细胞，骨细胞,和肌肉细胞在G1和G2。在ZG1和ZG2中，未观察到参数的显着变化（P>.05），并且没有组织病变。
■亚慢性GBH暴露损害钙稳态，观察到低钙血症，低维生素D,和继发性甲状旁腺功能亢进，引起甲状旁腺组织损伤，骨头,和大鼠的肌肉，这些被氯化锌预处理减轻。
