The aim of this study was to investigate the presence of mitochondrial DNA (mtDNA) alterations and metabolic dysfunctions in patients with presbyacusis, and to discover correlations between presbyacusis and the degree of hearing loss and mitochondrial damage. Seventy patients with presbyacusis were examined, including 40 Egyptian patients and 30 Italian patients. Forty eight normal subjects were included as control group, including 24 Egyptians and 24 Italians. There was no common point mutation, and A1555G, A3243G, A7445G not were detected in any patients or controls. Haplogroup U was significantly common in patients in comparison to controls. Mutation of antioxidant genes (GSTT1, GSTM1) were significantly present in only Italian patients compared to Italian controls.

The aim of this study was to investigate the presence of mitochondrial DNA (mtDNA) alterations and metabolic dysfunctions in patients with presbyacusis, and to discover correlations between presbyacusis and the degree of hearing loss and mitochondrial damage. Seventy patients with presbyacusis were examined, including 40 Egyptian patients and 30 Italian patients. Forty eight normal subjects were included as control group, including 24 Egyptians and 24 Italians. There was no common point mutation, and A1555G, A3243G, A7445G not were detected in any patients or controls. Haplogroup U was significantly common in patients in comparison to controls. Mutation of antioxidant genes (GSTT1, GSTM1) were significantly present in only Italian patients compared to Italian controls.

The aim of this study was to investigate the presence of mitochondrial DNA (mtDNA) alterations and metabolic dysfunctions in patients with presbyacusis, and to discover correlations between presbyacusis and the degree of hearing loss and mitochondrial damage. Seventy patients with presbyacusis were examined, including 40 Egyptian patients and 30 Italian patients. Forty eight normal subjects were included as control group, including 24 Egyptians and 24 Italians. There was no common point mutation, and A1555G, A3243G, A7445G not were detected in any patients or controls. Haplogroup U was significantly common in patients in comparison to controls. Mutation of antioxidant genes (GSTT1, GSTM1) were significantly present in only Italian patients compared to Italian controls.

Background and Aims Melatonin may be involved in gastrointestinal tract physiology and could affect inflammation-related gastrointestinal disorders. Rat models of ulcerative colitis imply melatonin is beneficial. To determine potential pathophysiological mechanisms, we assessed colonic nuclear factor-kappa beta expression and measured serum levels of pentraxin-3, lipid peroxides, and total thiols in an acetic acid model of this disease. Materials and Methods Thirty rats were divided into five groups: a control group, an acetic acid-induced colitis group, a group treated with melatonin before colitis induction, a group treated short-term after colitis induction, and a group treated long-term after colitis induction. After four weeks, blood samples were taken for measurement of pentraxin-3, lipid peroxide, and total thiols. Sections of the colon were taken for histopathological examination and immunohistochemical detection of nuclear factor-kappa beta expression. Results Melatonin administration reduced nuclear factorkappa beta immunohistochemical expression, reduced serum levels of lipid peroxide and pentraxin-3, and maintained serum levels of total thiols. However, in long-term treatment the protective effect of melatonin was not as marked. Conclusion Melatonin is effective in prevention and short-term treatment of the inflammatory process in aceticacid induced colitis whereas the benefit of long-term treatment is unclear. Benefit may be linked to protection mechanisms against inflammatory processes by inhibiting the nuclear factor-kappa beta and conserving endogenous antioxidant reserves of total thiols, thus reducing the level of colonic damage possibly caused by lipid peroxides.