Long-Term Exposure to Inorganic Mercury Leads to Oxidative Stress in Peripheral Blood of Adult Rats.

Mercury chloride (HgCl2) is a compound found in the environment that presents low risk due to low liposolubility. Considering the importance of blood as access rout to the systemic distribution of this toxicant to the organism as well as functions performed by it, this study aimed to investigate the effects of HgCl2 on the peripheral blood of rats, evaluating the oxidative biochemistry, blood count, and morphology of cell populations. For this, 20 adult Wistar male rats were divided into control (n = 10) and exposed (n = 10) groups and received distilled water or HgCl2 at a dose of 0.375 mg/kg for 45 days, respectively, through intragastric gavage. Then, the animals were euthanized and the blood was collected for total mercury (Hg) levels determination, complete blood and reticulocyte count, oxidative biochemistry by Trolox Equivalent Antioxidant Capacity (TEAC), reduced glutathione (GSH) levels, superoxide dismutase activity (SOD), thiobarbituric acid reactive substances (TBARS), and nitric oxide (NO), in blood cells and plasma. Long-term exposure increased total Hg in plasma and blood cells. In blood cells, only TEAC has decreased; in plasma, the HgCl2 increased TBARS and NO levels, followed by a decrease in TEAC and GSH levels. There were no quantitative changes in reticulocytes, erythrocytes, and hemoglobin; however, the number of leukocytes have increased and platelets have decreased. Our results suggest that even in the face of low toxicity when compared with other mercury species, HgCl2 at low doses is able to modulate the systemic redox balance and affect some blood cell populations.

Aluminum-Induced Toxicity in Salivary Glands of Mice After Long-term Exposure: Insights into the Redox State and Morphological Analyses.

Several studies indicate aluminum (Al) as a potent toxicant, mainly related to central nervous system disorders. However, investigations about the Al effects over salivary glands are still scarce. In this way, the present study aimed to investigate whether the Al chloride (AlCl3) is able of triggering oxidative stress in parotid and submandibular glands of mice and also, if any morphological impairment is observed. For this, twenty mice were divided into two groups: Exposed group (EG), which received 18.5 mg/kg of AlCl3 by intragastric gavage for 60 days and control group (CG), which received distilled water by intragastric gavage during the same period of time. After that, levels of reduced glutathione (GSH) and malonaldehyde (MDA) were analyzed and we performed morphological analyses by evaluating the area of parenchyma, stroma, acini, and ducts in both glands. Statistical analyses were performed by Student's t test and two-way ANOVA, adopting p < 0.05. No abnormal body weight was observed and data indicates that although both major salivary glands are susceptible to Al-induced oxidative stress, by increasing MDA and reducing GSH, only submandibular glands decreased the parenchyma and increased stroma area. Moreover, the submandibular glands showed smaller total area of acini and higher total area of ducts, in comparison with the control group. Notably, AlCl3 induces oxidative stress in both glands, however, submandibular glands showed to be more susceptible to Al effects than parotid glands. Our study gives evidences about Al toxicity in parotid and submandibular glands and claims for new investigations to understand more mechanisms of Al-induced toxicity.