Department of Biochemistry, Janaki Medical College and Teaching Hospital, Ramdaiya Bhawadi, Dhanusha, Nepal.
Department of Biochemistry, University of Allahabad, Allahabad 211002, India.
Anal Cell Pathol (Amst). 2018 May 29;2018:5028925. doi: 10.1155/2018/5028925. eCollection 2018.
Increased oxidative stress is a major cause of aging and age-related diseases. Erythrocytes serve as good model for aging studies. Dihydrotachysterol is known to induce premature aging feature in rats mimicking Hutchinson-Gilford progeria syndrome.
In the present study, attempts have been made to explore the differential response of young and senescent erythrocytes separated by density gradient centrifugation from accelerated senescence model of rats mimicking Hutchinson-Gilford progeria syndrome and naturally aged rats.
The erythrocytes of naturally aged and progeroid rats were separated into distinct, young and old cells on the basis of their differential densities. The parameters of oxidative stress and membrane transport systems were studied.
Our study provides evidence that organismal aging negatively affects oxidative stress markers and membrane transport systems in both young and old erythrocytes. This study further substantiates that the changes in progeria model of rats resemble natural aging in terms of erythrocyte senescence.
氧化应激增加是衰老和与衰老相关疾病的主要原因。红细胞是衰老研究的良好模型。二氢麦角固醇已知可诱导类似哈钦森-吉尔福德早衰综合征的大鼠过早衰老特征。
本研究试图探讨通过密度梯度离心从模拟哈钦森-吉尔福德早衰综合征的加速衰老大鼠模型和自然衰老大鼠中分离的年轻和衰老红细胞的差异反应。
根据红细胞的不同密度，将自然衰老和早衰大鼠的红细胞分为不同的年轻和衰老细胞。研究了氧化应激和膜转运系统的参数。
本研究提供的证据表明，机体衰老对年轻和衰老红细胞的氧化应激标志物和膜转运系统均有负面影响。这项研究进一步证实，大鼠早衰模型的变化在红细胞衰老方面与自然衰老相似。
