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近年，様々な疾病の発症要因の1つとして，生体成分の酸化的損傷の関与が知られるようになった．本研究では労働者の生活習慣に加えて，疲労の蓄積が，生体内酸化ストレスマーカーである尿中8-ヒドロキシデオキシグアノシン（8-OHdG）に与える影響について調査した．その結果，尿中8-OHdG値のアルコール摂取による上昇，間食摂取ならびに調査日前日の睡眠時間確保による低下を明らかにした．また，同一集団で1-2カ月後に再調査したところ，尿中8-OHdG値の低下が観察された．同時に行った生活習慣等に関するアンケート調査の中で，再調査時に変化が見られた項目は，直近1ヵ月勤務負荷の低下であった．疾病予防に向けた生活習慣の改善において，尿中8-OHdGの活用が今後期待される．, Oxidative stress in biological components has become recognized as one of the causative factors of various diseases. In this study, we investigated the effects of worker lifestyle and fatigue on the levels of urinary 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative stress. Our results revealed that urinary 8-OHdG level was increased by alcohol intake and decreased by snack intake and adequate sleep time on the day before the survey. A decrease in urinary 8-OHdG level was also observed in parallel with a decrease in workload. Urinary 8-OHdG monitoring is expected to be useful for disease prevention in the future.

【目的】糖尿病性腎症の発症・進展に酸化ストレスの関与が示されている.本研究では2型糖尿病モデルマウスC57BL/KsJ db/dbマウスを用いて,オキシカイン(Superoxide dismutase高含有南フランス産特別種メロン抽出物と小麦グリアジンの複合体)投与による糖尿病性腎症の進展抑制効果について評価した.【方法】6週齢雄C57BL/KsJ-db/dbマウスを対照食とオキシカイン混餌食で飼育し,18週齢まで経時的に体重,随時血糖,尿中アルブミン排泄量,尿中8-hydroxydeoxyguanosine(8-OHdG)の測定を行った.また,腎臓組織を用い8-OHdGの免疫組織化学により酸化ストレスを組織学的に評価した.【結果】両群において,随時血糖,体重増加量に有意な差は見られなかった.対照群では尿中アルブミンの増加とともに尿中8-OHdGの有意な増加を認め,免疫組織学的にも腎組織中8-OHdG陽性細胞数は有意に高値であった.【結論】糖尿病性腎症の発症進展抑制に,オキシカインが有用である可能性が示唆された., Oxidative stress is implicated as an important mechanism by which diabetes causes nephropathy. Oxykine is the cantaloupe melon extract rich in vegetal superoxide dismutase covered by polymeric films of wheat matrix gliadin. In this study, we examined whether chronic oral administration of oxykine could prevent the progression of diabetic nephropathy induced by oxidative stress using preclinical rodent model of type 2 diabetes. We used female db/db mice and their nondiabetic db/m littermates. The mice were divided into the following three groups: non-diabetic db/m; diabetic db/db, and diabetic db/db treated with oxykine. Blood glucose level, body weight, urinary albumin, and urinary 8-hydroxydeoxyguanosine (8-OHdG) were measured during the experiments. Histological and 8-OHdG immunohistochemical studies were preformed on 12 weeks from the beginning of treatment. After 12 weeks of treatment, the levels of blood glucose and the body weight were not significantly different between the oxykine-treated group and the non-treated db/db group, however both groups kept significantly high levels rather than db/m mice. The relative mesangial area calculated by mesangial area/total glomerular area ratio was significantly ameliorated in the oxykine treated group compared with non-treated db/db group. The increases in urinary albumin and 8-OHdG at 12 weeks of treatment were significantly inhibited by chronic treatment with oxykine. The 8-OHdG immunoreactive cells in the glomeruli of non-treated db/db mice were more numerous than that of oxykine-treated db /db mice. In this study, treatment of oxykine ameliorated the progression and acceleration of diabetic nephropathy for rodent model of type 2 diabetes. These results indicated that the oxykine reduced the diabetes-induced oxidative stress and renal mesangial cell injury. In conclusion, oxykine might be a novel approach for the prevention of diabetes nephropathy.