PubMed Health⌕ Search

Biomedical subjects

Mohinder P Bansal

Publications and source records attributed to Mohinder P Bansal.

10 recordsLinked to original sources

Role of selenium in spermatogenesis: differential expression of cjun and cfos in tubular cells of mice testis.

Selenium (Se) is an essential dietary trace element, involved in the process of male reproduction. Best known as an antioxidant, it acts through various selenoproteins viz. glutathione peroxidase, thioredoxin reductase and selenoprotein P. The aim of the present study was to identify the underlying molecular mechanism of Se in regulating spermatogenesis. Different Se status: deficient, adequate and excess Se, were generated in male Balb/c mice by feeding yeast based Se deficient diet, and deficient diet supplemented with Se as sodium selenite (0.2 and 1 ppm Se) respectively for a period of 4 and 8 weeks. Se levels and glutathione peroxidase (GSH-Px) activity were significantly reduced in the Se deficient mice and enhanced in Se supplemented group. Reduction in the number of post-meiotic germ cells viz. spermatids and spermatozoa, were observed in the deficient groups indicating loss in fertility and reproductive ability. cjun and cfos (components of transcription factor AP1) regulate cellular growth and differentiation and also exert a regulatory role in steroidogenesis and spermatogenesis. Changes in the mRNA expression of cjun and cfos were observed. Concomitant with this, western blot revealed that the protein expression profile for both these genes was significantly altered in the Se deficient and Se excess groups. Further immunohistochemical analysis showed that, both these genes had identical cellular localization indicating that they do not work alone but act synergistically as AP1. cjun and cfos expression was greater in the early mitotic stages-spermatogonia and spermatocytes in the Se adequate controls. It decreased in the meiotic stages and then again peaked around the later stages-elongating spermatids and spermatozoa. However in the Se deficient mice, weaker expression was observed in the spermatogonia with a complete absence of expression near the lumen. No visible changes in cjun/cfos expression and immunohistochemical localization were observed in the excess group compared to the Se adequate controls. In conclusion, the present study clearly demonstrates that alteration in Se supply leads to decreased expression pattern for both cJun and cFos in the testicular germ cells which might be responsible for decreased germ cell number, differentiation and reduced fertility and accounts for the mechanism of Se action in regulating spermatogenesis.

Animals↗

Effect of diethyl maleate induced oxidative stress on male reproductive activity in mice: redox active enzymes and transcription factors expression.

Free radicals and reactive oxygen species (ROS) associated with oxidative stress are likely to play a number of significant roles in male reproduction. Present study was carried out to evaluate the effect of diethyl maleate (DEM) induced oxidative stress on male fertility in mice. Intraperitoneal injection of DEM for two weeks resulted in decrease in reduced glutathione and increase in the oxidized glutathione levels in the testis. Effect on the reproductive ability in term of sperm concentration, motility and fertility status was studied. Sperm concentration and motility were found to be significantly reduced along with a significant reduction in the litter size. Expression of redox sensitive transcription factor, cjun and cfos genes, along with gamma-glutamyl cysteine synthetase (GCS) and manganese superoxide dismutase (MnSOD) expression were also studied using RT-PCR after DEM treatment. RT-PCR analysis revealed decrease in the testicular mRNA expression for cjun and cfos whereas the expression for GCS and MnSOD increased. Enzyme activity of SOD also increased. The study reflects the effect of DEM induced oxidative stress on the reproductive ability of male mice and interplay of the various components of the antioxidant defense system and redox regulated transcription factors at the transcriptional level.

Animals↗

Hypercholesterolemia and tissue-specific differential mRNA expression of type-1 5'-iodothyronine deiodinase under different selenium status in rats.

Type-1 5'-iodothyronine deiodinase (5'-DI) is responsible for conversion of T4 to T3. Selenium (Se) is an integral part of this enzyme. Keeping in view the strong association between atherosclerosis and hypothyroidism, the present study examined the behavior of 5'-DI in liver, aorta and thyroid during hypercholesterolemia following different Se status, i.e., Se deficiency (0.02 ppm), adequate (0.2 ppm) and excess dose (1 ppm) in SD male rats. Animals were fed a control or high-cholesterol diet (2%) for 1 and 2 months. 5'-DI activity and mRNA expression was measured by RIA and RT-PCR respectively. In liver and aorta, 5'-DI expression significantly decreased with the Se-deficient and the high-cholesterol diet. The trend was opposite in thyroid, i.e., mRNA expression increased significantly during selenium deficiency and with a high-cholesterol feeding. But with 1 ppm Se supplementation, the 5'-DI expression increased in all the three tissues. The present study indicates that hypercholesterolemia along with selenium deficiency is co-responsible for differential regulation of 5'-DI enzyme in thyroidal vs. extrathyroidal tissues. Distinct regulation of 5'-DI in the thyroid reflects the clinical importance of this selenoprotein during hypercholesterolemia as this enzyme is essential for T3 production, which further has a vital role in the maintenance of lipid metabolism.

Animals↗

Tertiary-butyl hydroperoxide induced oxidative stress and male reproductive activity in mice: role of transcription factor NF-kappaB and testicular antioxidant enzymes.

Reactive oxygen species (ROS) have been proposed as a major factor affecting male reproductive capacity. The present study has evaluated the possible role of oxidative stress during testicular pathogenesis in male mice exposed to tertiary-butyl hydroperoxide (TBHP). TBHP was administered by daily intraperitoneal injection for 2 weeks. Treatment greatly increased lipid peroxidation in the testis and led to a significant decrease in sperm concentration and motility and a reduction in litter size relative to controls. An increase in testicular mRNA abundance of redox-regulated p50 and p65 subunits of NF-kappaB was observed after TBHP treatment. Evaluation of NF-kappaB regulated antioxidant enzymes in the testis revealed an increase in superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) activities and corresponding mRNA abundance. These results suggest a potential role of NF-kappaB in oxidative stress mediated changes in the physiology of male reproductive system.

Animals↗

Modulation of hypercholesterolemia-induced alterations in apolipoprotein B and HMG-CoA reductase expression by selenium supplementation.

Various studies demonstrated a significant association between the trace element selenium (Se), hypercholesterolemia and the risk of cardiovascular disorders. Present study was aimed to reveal the role of Se supplementation in modulation of hypercholesterolemia-induced changes in apolipoprotein B (apoB) and 3-hydroxy 3-methylglutaryl co-enzyme A (HMG-CoA) reductase expression during experimental hypercholesterolemia in Sprague-Dawley male rats. Animals were fed 0.2 and 1 ppm Se-supplemented control diet as well as 2% cholesterol-supplemented diet for 3 months. Apolipoprotein B levels were measured by ELISA and Western blot. HMG-CoA reductase mRNA expression was studied by RT-PCR. ApoB levels increased significantly on 2% cholesterol-supplemented diet feeding. On 1 ppm Se supplementation apoB levels decreased significantly. HMG-CoA reductase mRNA expression decreased significantly on cholesterol-supplemented diet feeding and on 1 ppm Se supplementation the mRNA expression further decreased. So the present results demonstrate that 1 ppm Se supplementation is responsible for down regulation of apoB and HMG-CoA reductase expression during hypercholesterolemia. These findings highlight the therapeutic potential of selenium supplementation in lipid metabolism.

Animals↗

Hypercholesterolemia and LDL receptor mRNA expression: modulation by selenium supplementation.

Selenium (Se) status has been associated with cardiovascular disorders. Present study was aimed to elucidate the protective role of Se supplementation on LDL receptor (LDL-R) activity as well as mRNA expression during experimental hypercholesterolemia in SD male rats. Animals were fed 0.2 and 1 ppm Se supplemented control diet as well as 2% cholesterol supplemented diet for 3 months. LDL-R activity was measured in-vivo by injecting radiolabeled LDL to rats and decrease in counts per minute with time was taken as a measure of LDL clearance and in turn LDL-R activity. LDL-R mRNA expression was studied by RT-PCR. LDL-R activity and mRNA expression decreased significantly on 2% cholesterol supplemented diet feeding. On 1 ppm Se supplementation LDL-R activity as well as mRNA expression increased significantly. Present results demonstrate that Se supplementation upto 1 ppm is responsible for up regulation of LDL-R activity as well as mRNA expression, during hypercholesterolemia. These findings highlight the therapeutic potential of Se supplementation in lipid metabolism.

Animals↗

Attenuation of LDL receptor gene expression by selenium deficiency during hypercholesterolemia.

Selenium deficiency has been associated with hypercholesterolemia. Present study was aimed to determine the effect of selenium (Se) deficiency on LDL receptor (LDL-R) activity as well as mRNA expression during experimental hypercholesterolemia in SD male rats. Animals were fed Se adequate (0.2 ppm) and deficient (0.02 ppm) control diet as well as high cholesterol (2%) diet (HCD) for 1 and 2 months. LDL-R activity was measured in vivo by injecting radiolabeled LDL to rats and percent decrease in cpm with time was taken as a measure of LDL clearance and in turn LDL-R activity. LDL-R mRNA expression was studied by RT-PCR. LDL-R activity and mRNA expression decreased significantly on HCD feeding in both Se deficient and adequate diet fed rats after 2 months. In Se deficiency receptor activity and mRNA expression decreased significantly. After 2 months LDL-R activity and expression decreased in both the Se deficient groups and in Se adequate HCD fed group in comparison to 1 month data. But after 4 month there was no significant difference observed in LDL-R activity and mRNA expression in selenium deficiency as well as on HCD feeding. So the present results demonstrate that Se deficiency act synergistically with hypercholesterolemia to downregulate LDL-R activity as well as mRNA expression.

Animals↗

Hypercholesterolemia and apolipoprotein B expression: regulation by selenium status.

BACKGROUND: Apolipoprotein B (apoB) contains ligand-binding domain for the binding of LDL to LDL-R site, which enables the removal of LDL from circulation. Our recent data showed that selenium (Se) is involved in the lipid metabolism. The present study was aimed to understand the effect of Se deficiency (0.02 ppm) and selenium supplementation (1 ppm) on apoB expression in liver during hypercholesterolemia in male Sprague Dawley rats. Animals were fed with control and high cholesterol diet (2%) for 1 and 2 months. ApoB levels by ELISA and protein expression by western blot was done. Hepatic LDL receptor (LDL-R) activity (in vivo) and mRNA expression by RT-PCR was monitored. RESULTS: In selenium deficiency and on high cholesterol diet (HCD) feeding apoB levels increased and LDL-R expression decreased significantly after 2 months. On 1 ppm selenium supplementation apoB expression significantly decreased and LDL-R expression increased after 2 months. But after one month of treatment there was no significant change observed in apoB and LDL-R expression. CONCLUSION: So the present study demonstrates that Se deficiency leads to up regulation of apoB expression during experimental hypercholesterolemia. Selenium supplementation upto 1 ppm leads to downregulation of apoB expression. Further, this study will highlight the nutritional value of Se supplementation in lipid metabolism.

Animals↗

Effect of selenium-induced oxidative stress on the cell kinetics in testis and reproductive ability of male mice.

OBJECTIVE: The present study evaluated the role of experimental oxidative stress (induced by feeding diets with different concentrations of selenium [Se], a trace nutrient and potent antioxidant) on male reproductive activity in mice. METHODS: To create different levels of oxidative stress in male mice, three diets with different levels of Se were fed to different groups for 8 wk. Mice in group 1 were fed a yeast-based diet, which is considered a Se-deficient diet (0.02 ppm). Mice in groups 2 and 3 were fed with an Se-deficient diet supplemented with 0.2 and 1 ppm Se as sodium selenite, respectively. RESULTS: After completion of the feeding schedule, a significant decrease in Se levels were observed in Se-deficient mice (group 1), whereas Se levels greatly increased in the Se-excess mice (group 3). Glutathione peroxidase activity was greatly decreased in the liver and testis in group 1, whereas glutathione-S-transferase activity was significantly increased in the testis. No significant change was found in activities of glutathione peroxidase and glutathione-S-transferase in group 3 compared with group 2. Cell kinetics showed a significant decrease in the number of pachytene spermatocytes and young and mature spermatids in group 1 compared with group 2. No appreciable change was observed in the germinal cell population in group 3. A significant decrease in sperm number was observed in group 1 compared with group 2. No change in these parameters was observed in group 3. The fertility status of mice in terms of percent fertility and litter size also exhibited a significant decrease in the reproductive ability of group 1. No change in these parameters was observed in group 3 compared with group 2. CONCLUSION: The present results clearly demonstrate the effect of oxidative stress generated by feeding different concentrations of Se on cell kinetics in the testis and, hence, its effect on the reproductive ability of male mice.

Animals↗

Effect of experimental oxidative stress on steroidogenesis and DNA damage in mouse testis.

The objective of the present study was to evaluate the effect of oxidative stress induced by feeding various levels of selenium on steroidogenesis and DNA damage in mouse testes. To create various levels of oxidative stress in mice, diets with three different Se levels were fed to separate groups for 8 weeks. Group 1 animals were fed a yeast-based diet, which was considered a Se-deficient diet (0.02 ppm). Group 2 and 3 animals were fed a Se-deficient diet supplemented with 0.2 and 1 ppm Se as sodium selenite, respectively. After completion of the diet feeding, estimations were carried out, and results were compared with those of group 2. A significant decrease in Se levels was observed in group 1 animals, whereas they were greatly enhanced in group 3. Glutathione peroxidase (GSH-Px) activity was greatly reduced in both the liver and testes in group 1, whereas no significant changes were found in GSH-Px activity in group 3. Serum luteinizing hormone, follicle-stimulating hormone (FSH), and testosterone levels were reduced in group 1. Significant decreases of sperm number and motility were observed in group 1 when compared to group 2 male mice. No changes in these parameters were observed in group 3. DNA fragmentation was observed in both groups 1 and 3; however, the damage was more prevalent in group 1. The results clearly demonstrate the effect of oxidative stress generated by feeding various Se levels on the steroidogenesis and DNA fragmentation in mice testes.

Animals↗