Effect of chronic fluorosis on lipid peroxidation and histology of lung tissues in first and second generation rats

Abstract

This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first and second generation rat lung tissues. Sixteen, virgin, female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two experimental groups (control and fluoride supplemented). The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and lactation periods. After the lactation period, young animals (first generation; F1) were exposed to the same amount of NaF in drinking water for four months. At the end of the four-month experimental period, nine randomly-chosen male rats (F1) were sacrificed and lung tissues were removed for histopathological and enzymatic lipid peroxidation examination. The second generation rats were obtained from the remaining rats by the same method. They were also treated similarly. At the end of the four-month experimental period, nine randomly-chosen male rats (F2) were sacrificed, and the lungs were removed for histological and lipid peroxidation examination. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and the lung TBARS levels of fluoride supplemented F1 and F2 rats were higher than controls. There were marked histological changes in the lung tissues of fluoride supplemented F1 and F2 rats, as follows: in F1 rats; loss of alveolar architecture, emphysematous areas, descuamation of alveolar epithelium and alveolar congestion were observed. There were thickened interalveolar septae and congestion of alveolar septal vessels. Intraparenchymal thick-walled vessels were also observed. There were markedly perivascular and intraparenchymal focal mononuclear cell infiltrations. In F2 rats, in addition to these changes, there were lipid cell hyperplasia and increased connective tissue mass in the parenchymal areas. It is concluded that chronic fluorosis causes a marked destruction in lung tissues of F1 and F2 rats by causing lipid peroxidation.

Cerebral Epiphyseal Proteins and Melatonin Modulate the Hepatic and Renal Antioxidant Defense of Rats

“…Markers of oxidative stress damage can be found in many disease states including renal damage, chronic heart disease, and liver disease [28, 29]. Thus, excess free radical formation is associated with many disease states.…”

Experimental research Lung damage after long-term exposure of adult rats to sodium fluoride

“…The chronic fluorosis group (group I) was characterized by the presence of marked pathological effects on the lung. This destructive effect might be attributed to the effect of lipid peroxidation [8]. The increase in the level of lipid peroxides is associated with the decrease in the activities of superoxide dismutase, catalase, and glutathione peroxidase [11].…”

“…Another possible explanation for the destructive effect of chronic fluorosis intoxication is the alteration of antioxidant status, which may increase generation of free radicals [11]. Such free radicals affect cellular components such as lipids, proteins, DNA and carbohydrates [8]. …”

“…Marked destruction of lung tissue in the form of loss of alveolar architecture, emphysematous areas, desquamation of alveolar epithelium and alveolar congestion was documented [8]. Hyperaemia, necrosis of epithelial cells, numerous macrophages in interalveolar septa, infiltrations in the area of blood vessels and emphysematous blebs were also reported [1].…”

Analysis of metallic traces from the biodegradation of endomedullary AZ31 alloy temporary implants in rat organs after long implantation times

“…Chronic fluorosis is a slow and progressive process causing symptoms related to muscle-skeletal and dental systems. Damage caused by chronic fluorosis has also been reported in many tissues including the kidney, liver and brain (Oncu et al, 2006). For this reason, F accumulation in these organs has also been studied (Fig.…”