补充锌对Wistar大鼠亚慢性口服草甘膦除草剂(GOBARA®)引起的钙稳态、甲状旁腺、骨骼和骨骼肌组织学变化的影响

IF 1.9 Q3 PATHOLOGY Clinical Pathology Pub Date : 2024-07-26 eCollection Date: 2024-01-01 DOI:10.1177/2632010X241265854
Emmanuel Vandi Tizhe, Ikechukwu Onyebuchi Igbokwe, Celestine Onwu-Ibe Njokwu, Mohammed Yakasai Fatihu, Ussa Delia Tizhe, Najume Dogon-Giginya Ibrahim
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引用次数: 0

摘要

研究目的本研究旨在评估补锌对亚慢性口服草甘膦除草剂(GBH,GOBARA®)毒性暴露大鼠钙稳态、甲状旁腺、骨骼和骨骼肌组织学变化的影响:将 60 只雄性 Wistar 大鼠分成 6 组(DW、Z、G1、G2、ZG1、ZG2):DW和Z分别接受2 mL/kg蒸馏水和50 mg/kg氯化锌(2%);G1和G2分别接受187.5 mg/kg和375 mg/kg草甘膦(以GBH计);ZG1和ZG2在接受草甘膦前接受50 mg/kg氯化锌预处理,1小时后分别接受187.5 mg/kg和375 mg/kg草甘膦。每天灌胃一次,连续治疗 16 周。对血清钙、维生素 D 和副激素进行了估计。对甲状旁腺、股骨头和股二头肌进行了组织病理学检查:GBH暴露导致G1血清钙浓度显著下降(P = .0038),G1血清维生素D浓度显著下降(P = .0337),与DW相比,G1(P = .0168)和G2(P = .0079)副激素显著增加。与 DW 相比,G2 的其他参数没有发生明显变化(P > .05)。比较 G1 和 G2 后,未观察到 GBH 暴露的剂量依赖效应。在 G1 和 G2 中,甲状旁腺细胞、骨细胞和肌肉细胞发生了坏死性变化。在 ZG1 和 ZG2 中,没有观察到参数的显著变化(P > .05),也没有组织病变:结论:亚慢性 GBH 暴露会损害钙稳态,表现为低钙血症、低维生素 D 血症和继发性甲状旁腺功能亢进,并导致大鼠甲状旁腺、骨骼和肌肉组织损伤,而氯化锌预处理可减轻这些损伤。
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Effect of Zinc Supplementation on Altered Calcium Homeostasis, Parathyroid Gland, Bone, and Skeletal Muscle Histology Induced by Subchronic Oral Exposure to Glyphosate-Based Herbicide (GOBARA®) in Wistar Rats.

Objectives: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

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Clinical Pathology
Clinical Pathology PATHOLOGY-
CiteScore
2.20
自引率
7.70%
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66
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