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Effects of lead exposure on salivary glands of rats: insights into the oxidative biochemistry and glandular morphology.

Géssica de Oliveira LopesWalessa Alana Bragança AragãoPriscila Cunha NascimentoLeonardo Oliveira BittencourtAna Carolina Alves OliveiraLuana Ketlen Reis LeãoSergio Melo Alves-JúniorJoão de Jesus Viana PinheiroMaria Elena Crespo-LopezRafael Rodrigues Lima
Published in: Environmental science and pollution research international (2020)
This study aimed to investigate the effects of lead (Pb) exposure on parotid and submandibular glands through morphological aspects as well as the systemic and salivary gland redox state. Male Wistar rats were exposed to 50 mg/kg/day of Pb-acetate or distilled water by intragastric gavage for 55 days (n = 40). Blood samples were used for lipid peroxidation (LPO), glutathione (GSH), and trolox equivalent antioxidant capacity (TEAC) assays. Samples of salivary glands were analyzed by LPO, nitrites (NO), and antioxidant capacity against peroxyl radicals (ACAP) levels. Morphometric analyses (total stromal area [TSA], total parenchyma area [TPA], total ductal area [TDA], and total acinar area [TAA]) and immunohistochemistry for cytokeratin-19 (CK-19), metallothionein I/II (MT I/II), and anti-smooth muscle actin (α-SMA) were performed. The results revealed that exposure to Pb triggered systemic oxidative stress represented by lower GSH levels and increased TBARS/TEAC ratio in blood plasma. ACAP was reduced, while NO and LPO were increased in both parotid and submandibular. The morphological analyses showed increase on MT I/II expression, reduced CK-19 expression in both glands, and α-SMA reduced the immunostaining only in the parotid glands. The morphometric analyses revealed an increase in TPA in both glands, while TAA was reduced only in submandibular glands and TDA was increased only in parotid glands. Our findings are pioneer in showing that long-term exposure to Pb is able to promote blood and glandular oxidative stress associated with cellular, morphological, and biochemical damage in both parotid and submandibular glands.
Keyphrases
  • oxidative stress
  • heavy metals
  • smooth muscle
  • poor prognosis
  • dna damage
  • signaling pathway
  • ischemia reperfusion injury
  • induced apoptosis
  • fatty acid
  • aqueous solution