http://nopr.niscpr.res.in/handle/123456789/65673 2026-10-10T10:04:38Z http://nopr.niscpr.res.in/handle/123456789/65683 Title: Insight into the etiology of preeclampsia Authors: Kumar Das, Subir Abstract: Ample amount of dietary aliments and inhaled oxygen transmission by the placenta and uterus blood stream is necessary by the mother and emerging fetus for their good health. Delicate equilibrium among the angiogenic growth activators and its receptors are responsible to reshape the spiral arteries, neoangiogenesis and the fetus development. Abnormal placentation in the beginning of pregnancy causes flawed reshaping the vessels of the uterus and releases numerous biological molecules in the maternal circulatory system, obstructing the balance among proangiogenic growth factors, such as, vascular endothelial growth factor (VEGF) or placental growth factor (PlGF) with antiangiogenic factors, like soluble form of fmslike tyrosine kinase-1 (sFlt-1) or endoglin (s-Eng). Inadequate placentation also secrete proinflammatory cytokines (such as TNF-), oxygen deprived hypoxia-inducible factor (HIF), unstable reactive oxygen and nitrogen species (RONS), and autoantibodies against angiotensin type 1 receptors. There is also reduced generation of vasodilators, such as, nitric oxide (NO) and/ or prostacyclin. These alterations leading to inflammatory response, endothelial dysfunction and glomerular damage. Comorbidities present in mother, such as hypertension, diabetes mellitus, kidney ailments, antiphospholipid antibody syndrome, overweight, aging, or, a family history of pregnancy disorders are some of the notable risk factors. The vasculatures present in both placenta and maternal are important sources of RONS, a source of powerful pro-oxidants that can modify biomolecules and changes vascular activities in preeclampsia (PE). The sFlt-1/PlGF ratio is considered as an important risk identifier of PE development. Several therapeutics approaches are considered targeting angiogenic factors to treat preeclampsia; yet, placenta delivery is the ultimate definitive treatment. Page(s): 449-456 2025-04-01T00:00:00Z http://nopr.niscpr.res.in/handle/123456789/65682 Title: Existence of differential epigenetic control in a pair of cultivated tobacco (Nicotiana tabacum L.) cultivars harbouring contrast nicotine levels Authors: Manoharlal, Raman; Saiprasad, GVS Abstract: Nicotine (NIC) is a primary and characteristic alkaloid in tobacco (Nicotiana sp.). To date, there have been no comprehensive studies conducted to assess the prevalence of epigenetic phenomena related to tobacco NIC levels. Therefore, our present research seeks to investigate the potential prevalence of two significant epigenetic markers, specifically chromatin organization and genomic DNA (gDNA) methylation, in relation to physiological levels of NIC in tobacco. Our agronomical-field studies on the cultivated tobacco (N. tabacum L.) germplasm collection screening revealed a contrast pair of tobacco cv., GP150 and GP98,that exhibit consistent differences in their inherent NIC levels. GP150 harbors inherently high-NIC levels in its green- [~1.27% d.w. (pre-topping) and 2.87% d.w. (post-topping)] and cured-leaves (~3.01% d.w.). On the contrary, GP98 harbors inherently low-NIC levels in its green- [~0.04% d.w. (pre-topping) and 0.07% d.w. (post-topping)] and cured-leaves (~0.09% d.w.). A comparative evaluation of epigenetics phenomenon revealed that GP150 and GP98 differ significantly in terms of: (1) chromatin organization, (2) gDNA methylation status, (3) gDNA 5-methylcytosine (5mC) levels and (4) gDNA methyltransferases activity. An induced physiological alteration in gDNA methylation corroborated with corresponding alterations in NIC level further substantiates an intriguing correlation between aforementioned epigenetics phenomenon(s) and NIC biosynthesis in tobacco. These results reinforce the need of future in-depth epigenetics studies on NIC biosynthesis and/ signalling pathways in tobacco. Page(s): 457-468 2025-04-01T00:00:00Z http://nopr.niscpr.res.in/handle/123456789/65681 Title: Impact of lead acetate oral administration on wistar rat lung health: Histological evaluation Authors: Phillips Akano, Oyedayo; Adebola Adetunji, Opeyemi; Soneye, Oluwafeyisola; Olufunso Adeoye, Bayo; Oluwadunsin Adebayo, Iyanuoluwa; David Adeoye, Ayodeji; Tunde Ogunsanya, Sanmi; Lina Nwobi, Nnena; Akinnawo, Olubukola; Joseph Nwobi, Chigbogu; Bangsi Achor, Corniluis; Adeyemi, Samson; Temitope Adebayo, Barakat; Dada, Moyosoluwa Abstract: Lead, a pervasive heavy metal, poses significant health risks to various bodily functions, including respiratory health. In this study, we aimed to investigate the impact of lead acetate exposure on lung histoarchitecture and glycogen levels in male Wistar Albino rats. The primary objective of this study was to assess the effects of lead acetate on lung histoarchitecture and glycogen levels in male Wistar Albino rats. Specifically, we aimed to determine the dose-dependent changes in lung morphology and glycogen content following oral administration of lead acetate solutions. Forty mature male albino rats were divided into four groups: a control group receiving clean water and pelletized feed, and three experimental groups receiving lead acetate solutions orally at doses of 50 mg/kg, 100 mg/kg, and 150 mg/kg body weight for 35 days. At the end of the experimental period, lung tissues were harvested, fixed in normal saline, and subjected to histological examination using routine hematoxylin and eosin staining to assess lung histoarchitecture. Additionally, Periodic Acid-Schiff (PAS) reaction was employed to demonstrate glycogen levels in the lung tissues. Histological analysis revealed significant alterations in lung histoarchitecture in the experimental groups compared to the control group, including inflammation, fibrosis, and cellular damage. Furthermore, lead acetate exposure led to a dose-dependent decrease in glycogen levels within lung tissues. Our findings demonstrate the detrimental impact of lead acetate on lung histoarchitecture and glycogen levels in male Wistar Albino rats. These results underscore the importance of mitigating environmental exposure to lead to preserve respiratory health. Further research is needed to elucidate the underlying mechanisms of lead-induced lung toxicity and explore potential therapeutic interventions. Page(s): 469-479 2025-04-01T00:00:00Z http://nopr.niscpr.res.in/handle/123456789/65680 Title: Lipid peroxidation level and histological changes in rat liver after the cisplatin and dexamethasone separate and combined action Authors: Yavroyan, Zhenya; Hakobyan, Nune; Hovhannisyan, Agapi; Grigoryan, Anna; Karapetyan, Anna; Abgaryan, Tamara; Gevorgyan, Emil Abstract: Cisplatin is known to exhibit pro-oxidative properties, which are responsible for various toxicities caused by this drug, including hepatotoxicity. Dexamethasone, which is known as anti-inflammatory and immunomodulatory drug, is used with cisplatin to mitigate its side effects. However, dexamethasone, like other glucocorticoids, can induce oxidative stress and lipid peroxidation processes. In addition, it is known that dexamethasone causes liver damage and hepatotoxicity. The aim of this study was to clarify how dexamethasone, having a similar effect to cisplatin, alleviates the side effects caused by this antitumor drug. Our studies have shown that cisplatin and dexamethasone increase the formation of lipid peroxidation products conjugated dienes and trienes of rat’s liver to varying degrees extent in the case of separate and combined injection. In addition, cisplatin and dexamethasone were shown to increase the amount of lipid peroxidation marker malondialdehyde (MDA), in the rat liver tissue homogenate after separate and combined administration. These changes, as well as a decrease in the activity of the antioxidant enzyme catalase, confirm the pro-oxidative nature of cisplatin and dexamethasone. Moreover, the histopathological studies also testify to their hepatotoxic effect. However, contrary to the expected synergistic enhancement of both lipid peroxidation processes, and histological changes, a reduction in cisplatin effect by dexamethasone was observed. Thus, it is hypothesized that this “deterrent” effect of dexamethasone, combined with its anti-inflammatory and immunomodulatory properties, allows mitigating the side effects of cisplatin. Page(s): 480-489 2025-04-01T00:00:00Z