ABSTRACT
The aim of this study was to evaluate the antimutagenic and antigenotoxic potential of grape juice concentrate in rodent organs exposed to cadmium chloride intoxication. A total of 15 Wistar rats were distributed into three groups (n = 5), as follows: control group (CTRL; nontreated group), cadmium group (Cd), and cadmium-grape juice group (Cd + GJ). Exposed animals received intraperitoneal injection of cadmium chloride (1.2 mg/kg body weight) diluted in water and, after 15 days, Cd + GJ group received grape juice concentrate for 15 days, by gavage (0.8 mL, 1.18 mg of polyphenols kg(-1) day(-1)). Grape juice concentrate was able to decrease genotoxic effects induced by cadmium in peripheral blood and liver cells as depicted by single cell gel (comet) and micronucleus assays. A decrease for anti-8-hydroxy-20-deoxyguanosine (8OHdG) expression in hepatocytes of animals exposed to cadmium and treated with grape juice concentrate was also detected. Higher CuZn-SOD activity was observed in liver cells of the Cd + GJ group. No remarkable differences were seen regarding Mn-SOD activity among groups. Taken together, our results demonstrate that grape juice concentrate was able to exert antimutagenic and antigenotoxic activities in blood and liver cells of rats exposed to cadmium.
Subject(s)
Antimutagenic Agents/pharmacology , Beverages , Cadmium Chloride/toxicity , Environmental Pollutants/toxicity , Plant Extracts/pharmacology , Vitis/chemistry , Animals , DNA Damage , Fruit/chemistry , Gene Expression/drug effects , Liver/drug effects , Liver/enzymology , Liver/pathology , Rats, Wistar , Superoxide Dismutase/genetics , Superoxide Dismutase/metabolismABSTRACT
The aim of this study was to evaluate the anti-tumor activity of grape juice concentrate following medium-term oral carcinogenesis assay induced by 4-nitroquinoline 1-oxide (4NQO). A total of 30 male Wistar rats were distributed into five groups, as follows (n = 6 per group): Group 1 - negative control group (non-treated group); Group 2 - received grape juice concentrate at 1% dose by gavage for eight consecutive weeks; Group 3 - received 4NQO for 8 weeks at 20 ppm dose in drinking water daily; Group 4 - received 4NQO at 20 ppm dose during 8 weeks in drinking water and treated with grape juice concentrate at 1% dose orally by gavage for first 4 weeks after 4-NQO administration; Group 5 - received 4NQO at 20 ppm dose for 8 weeks in drinking water and treated with grape juice concentrate at 1% dose orally by gavage between the 5th and 8th weeks daily. Histopathological analysis revealed a decrease in hyperplasic and dysplastic lesions in Group 4. Groups 4 and 5 showed decreased COX-2 and TNF-alpha and eNOS gene expression. Grape juice concentrate also increased SOD Cu/Zn and catalase expression. However, Ki-67 immunoexpression was reduced at the promotion step of oral carcinogenesis (G5). Taken together, our results demonstrate that grape juice concentrate modulates rat tongue carcinogenesis as a result of anti-inflammatory activity, antioxidant activity and down-regulation of oral cells proliferation.
Subject(s)
4-Nitroquinoline-1-oxide/toxicity , Anticarcinogenic Agents/pharmacology , Beverages , Tongue Neoplasms/prevention & control , Tongue/drug effects , Vitis , Animals , Base Sequence , Comet Assay , Cyclooxygenase 2/metabolism , DNA Primers , Male , Nitric Oxide Synthase Type III/metabolism , Polymerase Chain Reaction , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Tongue/enzymology , Tongue/metabolism , Tongue Neoplasms/chemically induced , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Muscle crush injury is a common trauma in the modern society after as a result of mass disasters after penetration into muscle by high-velocity projectiles, blunt external trauma, or by gravity during prolonged immobilization in comatose patients after head trauma, alcoholic or drug overdose. However, the underlying mechanisms linking these alterations are still not fully understood, especially in acute phase. The aim of this study was to analyze genomic instability in multiple organs of rats after acute muscle injury by means of single cell gel (comet) assay. Rats were randomly distributed into three groups (n=6 each group): control group and experimental groups: sacrificed 6h as 12h after muscle compression. These results indicate genetic damage in peripheral blood cells as depicted by tail moment results. DNA breakage was also detected in liver, lung and kidney cells after acute muscle injury for two times evaluated. Heart cells showed genetic damage after 12h following muscle compression. Taken together, our results suggest that acute muscle injury induces genomic damage in multiple organs of Wistar rats. This novel finding offers new insights into the underlying mechanisms of the relationship between acute crush muscle injury and clinical manifestations that can occur during limb compression.
ABSTRACT
Oral cancer is a common neoplasm worldwide. Its incidence and mortality have also increased over the past decades. It is characterized by poor prognosis and a low survival rate despite sophisticated surgical and radiotherapeutic modalities. Metastasis of oral cancer is a complex process involving detachment of cells from tumor tissue, regulation of cell motility and invasion, proliferation and evasion through the lymphatic system or blood vessels. In this review, we will focus on the current knowledge in metastasis from oral cancer regarding facts, such as incidence; stage, histopathology and grade of primary tumor; clinical manifestations; diagnosis; and treatment. Certainly, such information will contribute to the understanding of oral cancer pathogenesis.
