A comparison of the potential of melatonin and tryptophan to ameliorate CCl4-induced hepatic and renal toxicity in Wistar rats.

CCl4 causes oxidative injury, fatty degeneration, fibrosis of the liver, renal failure, and even hepatocellular and renal carcinoma. Certain substances have the potential to neutralize the harmful effects of CCl4, so it will lead to numerous beneficial effects. Melatonin (MEL) is a powerful antioxidant that regulates circadian rhythm and has beneficial effects on organism; tryptophan (TRP) is its precursor necessary for the synthesis of MEL. The aim of the current study was to determine whether MEL and TRP, have protective effects during subchronic application of CCl4 to the liver and kidneys. Results suggest that CCl4 led to decrease of total proteins, albumins, globulins, erythrocytes, hemoglobin, and hematocrit; and increase of creatinine, AST, ALT values, and leukocytes. MEL and TRP both showing protective effects on regulation of serum proteins, albumins, globulins, A/G, AST, ALT, and creatinine levels. TRP had been shown to have potential in regulation of disbalanced hematological parameters caused by CCl4. TRP had beneficial effects on hepatocyte morphology in term of beaded chromatin and preserved cell morphology. Overall, oral supplementation of TRP had better protective effects on liver/kidneys compared to MEL.

Chronic cadmium exposure in Japanese quails perturbs serum biochemical parameters and enzyme activity.

Cadmium is a heavy metal, toxic even in trace amounts and its biological function in the human body has not been described to date. It is assumed that cadmium manifests in dose-dependent genotoxic and cytotoxic effects on many organs and tissue types. In this study, we have analyzed the biochemical parameters in the serum of Japanese quails (Coturnix japonica) after chronic in vivo exposure to cadmium. Adult animals were exposed to cadmium in the form of CdCl2 dissolved in water (0.20 mg/L) for 20 days. Significant differences between controls and exposed animals were found in 12 out of 13 analyzed biochemical parameters. Total bilirubin concentrations did not show any significant differences between the two groups. Exposure to cadmium has resulted in a significant increase in lactate dehydrogenase activity, sodium and chloride concentration, as well as significant reductions in total proteins, albumins, globulins, glucose, triglycerides, cholesterol, calcium concentration, and alkaline phosphatase activity. In this sense, chronic in vivo exposure to low doses of cadmium has induced severe changes in the levels of observed biochemical parameters and enzyme activity. Additionally, evident cytogenetic changes in the liver were also noted, where hepatocyte damage and even lack of organized nuclei, including nuclear fragmentation, clearly indicated ongoing apoptotic processes.

Impairments of bone marrow hematopoietic cells followed by the sever erythrocyte damage and necrotic liver as the outcome of chronic in vivo exposure to cadmium: novel insights from quails.

Cadmium is a heavy metal classified as an environmental hazard, and its toxicity is subject to extensive research. Japanese quails were exposed to cadmium chloride (CdCl2) ad libitum for 20 days. Bone marrow, peripheral blood and liver were analyzed following the exposure. Moreover, we have provided the very first explanation of hematopoietic lines in Japanese quail. Following CdCl2 exposure, changes in the number, size and morphology of blood cells were observed in both peripheral blood and bone marrow. Alterations included severe erythrocyte damage, monocytosis and lymphopenia. In the liver of Cd-exposed animals we observed necrotic cells, absence of hematopoietic regions and cytogenetic changes of hepatocytes. Alterations in the bone marrow were also noted, as well as giant phagocytic cells, most likely macrophages. In vivo, CdCl2 exposure caused swift and destructive changes in the hematopoietic niche, liver and other tissues responsible for the detoxification cycle of cadmium and its compounds.