nematollah razmi

Monosodium glutamate (MSG) is known as a food flavor enhancer that can adversely affect the male reproductive system. The present study was investigated the protective effect of coenzyme Q10 (Co-Q10) against MSG-induced oxidative stress and histopathological changes in rat testicular tissue.

In this experimental study, 40 adult male Wistar rats were randomly divided into 4 groups including control, MSG, MSG + Q10-10 and MSG + Q10-20. MSG gavage (3 gr / kg) and Co-Q10 injection were performed at doses of 10 and 20 mg / kg (intraperitoneally) for 4 weeks. The activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) was determined by ELISA and malondialdehyde (MDA) by thiobarbituric acid techniques in testicular tissue. Then, histological evaluation of testicular tissue was performed in the groups.

Monosodium glutamate increased the level of lipid peroxidation along with a significant decrease in the activity of CAT, SOD and GPX enzymes in testicular tissue. Co-administration of Co-Q10 in MSG groups reduced lipid peroxidation, increased the activity of CAT, SOD and GPx enzymes. On the other hand, Co-Q10 significantly reduced MSG-induced histopathological changes in the testicular tissue of treated rats.

Co-Q10 supplementation can ameliorates MSG-induced testicular toxicity and reduce oxidative stress on testicular tissues.

The present study was performed to assess the effects of heat stress on on Malondialdehyde (MDA) levels and catalase (CAT), Glutathione Peroxidase (GPX) and Superoxide dismutase (SOD) activity of blood serum and liver in Rattus. In doing so, 15 specimens were assigned to 3 groups i.e. the control group (kept for 21 days at 24±1 C), the chronic stress group (kept for 21 days at 38±1 C), and the acute stress groups (kept for 20 days at 24±1 C+2 days at 38±1 C in four hr. intervals). At the end of the experiments 5cc cardiac blood was sampled from each specimen and oxidant/antioxidant factor levels (i.e. MDA, SOD, CAT, and GPX) were measured. Also, to measure these enzymes in liver tissue, this tissue was isolated and homogenized. The results showed that the amount of tissue malondialdehyde in all groups was significantly increased compared to its level in serum that in acute and chronic heat stress compared to the control group this increase was significant (p<0.05). This increase in serum glutathione peroxidase was also significant compared to the control group (p<0.05). There was a significant increase in the levels of catalase and superoxide dismutase enzymes in the acute stress group compared to the control group. In conclusion, heat stress seems to induce oxidative stress in Rattus.

Myocardial infarction (MI) is a multifactorial disease caused by the suspension of blood circulation in a part of the myocardium. Understanding the genetic basis of MI can provide insight regarding the pathogenesis of the disease. The aim of this study was to investigate the association between pathogenic mutations and early-onset MI in five families with familial MI and without common MI risk factor.

Patients with MI younger than 50 years with family history of MI and without common diagnostic criteria (obesity, diabetes, familial hypercholesterolemia, opium/alcohol use) were evaluated for pathogenic mutations by whole exome sequencing (WES) and mutation was confirmed by polymerase chain reaction (PCR)-Sanger sequencing.

The c.2855G>A missense mutation with homozygous autosomal recessive inheritance was identified in low-density lipoprotein receptor-related protein 8 (LRP8) gene in all patients of a family.

The c.2855G>A (R952Q) mutation in LRP8 gene in homozygous state could be considered as a possible etiology of early-onset familial MI.