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Introduction: Bipolar disorder is a type biphasic disorder of energy availability that indicates increased mitochondrial respiration in episodes of mania, compared to decreased mitochondrial function in the depressive phase of the illness. Mitochondrial dysfunction may lead to an excessive increase in reactive oxygen species (ROS). The UCP-2 proteins act as regulators of ROS in the cell. This study aimed to investigate the association of UCP-2 45bp ins/del genetic variant with susceptibility to bipolar disorder.
 
Materials & Methods: This case-control study was performed on 205 subjects with bipolar disorder and 200 healthy subjects as a control group. After extraction of DNA from peripheral blood samples, genotype determination was performed using the PCR method. Moreover, the logistic regression analysis was used for the comparison of genotypes and allele frequencies between case and control groups.
Ethics code: IR.SUMS.REC.1396.S435
 
Findings: There was a significant association between ID (OR=0.42; 95% CI= 0.27-0.64; P<0.001) and II (OR=0.39; 95% CI=0.20-0.77; P=0.006) genotypes with bipolar disorder. Data analysis showed I allele had a protective effect on susceptibility to bipolar disorder (OR=0.56; 95% CI=0.42-0.75; P<0.001).
 
Discussions & Conclusions: This study investigated, for the first time, the association between UCP-2 45bp ins/del genetic variant and bipolar disorder. The results showed UCP-2 45bp ins/del genetic variant was associated with bipolar disorder; however, more studies are required to be conducted in different ethnicities to confirm these results.

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Introduction: Increasing levels of free radicals in the ova reduce the quality of their fertilization. Investigations have revealed the elevated production of tissue and serum-free radicals in women with polycystic ovary syndrome. Sirtuin-3 is located in mitochondria and plays an important role in the deactivation of free radicals. This study aimed to investigate the expression of the Sirtuin-3 gene in the ova of polycystic ovary syndrome affected mice.
Material & Methods: Polycystic ovary syndrome was induced by the injection of estradiol valerate (40 mg/kg) in six NMRI mice (age: six weeks old; weight: 25±5); moreover, six mice were selected as a control group. Following the induction, the structure of the ovaries was examined using the histotechnique, and the serum levels of sex hormones were determined using ELISA. The ova were collected from the ovaries, and their RNA was extracted by a special kit and converted to cDNA. Real-Time PCR was performed to analyze the expression of Sirtuin-3, and the Gapdh gene was selected as an internal control.
(Ethic code: 97/6505)
Findings: In the mice with polycystic ovary syndrome, hydatid cysts were formed in the ovaries. Furthermore, serum FSH hormone levels decreased in the affected mice, while LH and testosterone levels elevated, compared to those in the control mice (P<0.001). The expression of Sirtuin-3 was reduced in the ova of mice with polycystic ovary syndrome, compared to that in healthy mice in the ratio of 0.18 (P<0.05).
Discussion & Conclusion: The result of the present study showed that the expression of the Sirtuin-3 gene was decreased in the ovum of mice with polycystic ovary syndrome. Moreover, the disrupted expression of the Sirtuin-3 in the ovum can be suggested as one of the causes of reduced quality of the ovum in patients with polycystic ovary syndrome.
 

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Introduction: The anti-cancer effects of silymarin have been reported in several studies. However, the mechanism of its action in colon cancer cells is not well understood. This study aimed to investigate the effect of silymarin on the mitophagy pathway and the formation of reactive oxygen species (ROS) in human colon cancer cells (HT-29).
Material & Methods: HT-29 cancer cells and NIH-3T3 non-cancer cells were exposed to 0 (control), 25, 50, and 100 μg/ml of silymarin for 48 h. Cell viability, ROS level, mitochondrial membrane potential (MMP), and expression of important mitophagy-related genes including Pink1 (PTEN-induced putative kinase protein 1) and Parkin were examined to evaluate the effects of silymarin.
(Ethic code: IR. AJUMS. CMRC-9503)
Findings: Silymarin significantly reduced the viability percentage of the HT-29 cells depending on the concentration (P<0.05). It also significantly decreased MMP in a concentration-dependent manner while significantly increased ROS formation in the HT-29 cells (P<0.05). In addition, silymarin significantly increased the expression of Pink1 and Parkin genes in a concentration-dependent manner (P<0.05). Concentration of 100 μg/ml of silymarin had the greatest effect on reducing viability and MMP, as well as increasing ROS levels and expression of mitophagy-related genes (P<0.001). Silymarin did not cause significant changes in the viability percentage, ROS level, and MMP of the NIH-3T3 non-cancerous cells at different concentrations.
Discussion & Conclusion: According to the results, silymarin increases the level of ROS by decreasing MMP, thereby inducing mitophagy through the Pink1/Parkin signaling pathway in the HT-29 cells.