Department Of Zoology
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Item A comprehensive review on the decabromodiphenyl ether (BDE-209)-induced male reproductive toxicity: Evidences from rodent studies(Elsevier B.V., 2023-08-02T00:00:00) Sarkar, Debarshi; Midha, Parul; Shanti, Shashanka Sekhar; Singh, Shio KumarPolybrominated diphenyl ethers (PBDEs), a class of brominated flame retardants (BFRs), are employed in various manufactured products to prevent fires, slow down their spread and reduce the resulting damages. Decabromodiphenyl ether (BDE-209), an example of PBDEs, accounts for approximately 82 % of the total production of PBDEs. BDE-209 is a thyroid hormone (TH)-disrupting chemical owing to its structural similarity with TH. Currently, increase in the level of BDE-209 in biological samples has become a major issue because of its widespread use. BDE-209 causes male reproductive toxicity mainly via impairment of steroidogenesis, generation of oxidative stress (OS) and interference with germ cell dynamics. Further, exposure to this chemical can affect metabolic status, sperm concentration, epigenetic regulation of various developmental genes and integrity of blood-testis barrier in murine testis. However, the possible adverse effects of BDE-209 and its mechanism of action on the male reproductive health have not yet been critically evaluated. Hence, the present review article, with the help of available literature, aims to elucidate the reproductive toxicity of BDE-209 in relation to thyroid dysfunction in rodents. Further, several crucial pathways have been also highlighted in order to strengthen our knowledge on BDE-209-induced male reproductive toxicity. Data were extracted from scientific articles available in PubMed, Web of Science, and other databases. A thorough understanding of the risk assessment of BDE-209 exposure and mechanisms of its action is crucial for greater awareness of the potential threat of this BFR to preserve male fertility. � 2023 Elsevier B.V.Item A deeper understanding about the role of uranium toxicity in neurodegeneration(Academic Press Inc., 2023-06-15T00:00:00) Vellingiri, BalachandarNatural deposits and human-caused releases of uranium have led to its contamination in the nature. Toxic environmental contaminants such as uranium that harm cerebral processes specifically target the brain. Numerous experimental researches have shown that occupational and environmental uranium exposure can result in a wide range of health issues. According to the recent experimental research, uranium can enter the brain after exposure and cause neurobehavioral problems such as elevated motion related activity, disruption of the sleep-wake cycle, poor memory, and elevated anxiety. However, the exact mechanism behind the factor for neurotoxicity by uranium is still uncertain. This review primarily aims on a brief overview of uranium, its route of exposure to the central nervous system, and the likely mechanism of uranium in neurological diseases including oxidative stress, epigenetic modification, and neuronal inflammation has been described, which could present the probable state-of-the-art status of uranium in neurotoxicity. Finally, we offer some preventative strategies to workers who are exposed to uranium at work. In closing, this study highlights the knowledge of uranium's health dangers and underlying toxicological mechanisms is still in its infancy, and there is still more to learn about many contentious discoveries. � 2023 Elsevier Inc.Item Concurrent Assessment of Oxidative Stress and MT-ATP6 Gene Profiling to Facilitate Diagnosis of Autism Spectrum Disorder (ASD) in Tamil Nadu Population(Springer, 2023-03-27T00:00:00) Vellingiri, Balachandar; Venkatesan, Dhivya; Iyer, Mahalaxmi; Mohan, Gomathi; Krishnan, Padmavathi; Sai Krishna, Krothapalli; Sangeetha, R.; Narayanasamy, Arul; Gopalakrishnan, Abilash Valsala; Kumar, Nachimuthu Senthil; Subramaniam, Mohana DeviAutism spectrum disorder (ASD) is a neurodevelopmental disability that causes social impairment, debilitated verbal or nonverbal conversation, and restricted/repeated behavior. Recent research reveals that mitochondrial dysfunction and oxidative stress might play a pivotal role in ASD condition. The goal of this case�control study was to investigate oxidative stress and related alterations in ASD patients. In addition, the impact of mitochondrial DNA (mtDNA) mutations, particularly MT-ATP6, and its link with oxidative stress in ASD was studied. We found that ASD patient�s plasma had lower superoxide dismutase (SOD) and higher catalase (CAT) activity, resulting in lower SOD/CAT ratio. MT-ATP6 mutation analysis revealed that four variations, 8865 G>A, 8684 C>T, 8697 G>A, and 8836 A>G, have a frequency of more than 10% with missense and synonymous (silent) mutations. It was observed that abnormalities in mitochondrial complexes (I, III, V) are more common in ASD, and it may have resulted in MT-ATP6 changes or vice versa. In conclusion, our findings authenticate that oxidative stress and genetics both have an equal and potential role behind ASD and we recommend to conduct more such concurrent research to understand their unique mechanism for better diagnosis and therapeutic for ASD. Graphical Abstract: [Figure not available: see fulltext.] � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item Herbal Remedies for Improving Cancer Treatment Through Modulation of Redox Balance(Springer Singapore, 2022-09-28T00:00:00) Kaur, Sukhchain; Verma, Harkomal; Kaur, Sharanjot; Singh, Subham; Mantha, Anil K.; Dhiman, MonishaThe redox modulation induced by oxidative stress is one of the major cause of the metabolic and inflammatory disorders including cancer. The reactive oxygen species (ROS) produced by various sources in the cell shift the redox homeostasis of cells towards more oxidizing or acidic environment. This shift results in the alterations of normal physiologic functioning of biomolecules as well as causes damage to these biomolecules (proteins, lipids, and DNA/RNA). The excessive ROS and redox modulation are the key factors that support growth, progression, and survival of cancer cells. ROS-induced redox modulation further activates pro-tumorigenic cellular pathways for e.g., PI3K/AKT, HIF-1, and MAPK signaling pathways as well as hinders epigenetic signaling. Increasing evidences demonstrate that long-term side effects of anti-cancer chemotherapy are major concern of medical sciences although modern treatments are quite effective. The combination of various herbal formulations with anti-cancer therapy shows improvement in treatment effectiveness in cancer patients. Bioactive compounds present in herbal formulations possess antioxidant and anti-cancer properties that help in the regulation of redox status of cancer cells. The synergetic effects of herbal remedies along with conventional treatment are proven as novel therapeutics in cancer progression management. Clinical studies have shown that broad range of herbs and bioactive compounds from various plants having antioxidant, anti-inflammatory properties can suppress the carcinogenesis. In this chapter we will discuss the role of various plants such as Glycyrrhiza glabra, Picrorhiza kurroa, Tinospora cordifolia, Curcuma longa, Ocimum sanctum, Viola odorata, and bioactive compound ferulic acid found in various cereals. The chapter will also focus on various mechanisms involved in the modulation of chemo-toxicity and improvement of efficacy of conventional anti-cancer therapies by these plants. � Springer Nature Singapore Pte Ltd. 2022.Item Decabromodiphenyl ether (BDE-209) exposure to lactating mice perturbs steroidogenesis and spermatogenesis in adult male offspring(Academic Press, 2020-12-29T00:00:00) Sarkar, Debarshi; Singh, Shio KumarDecabromodiphenyl ether (BDE-209) is widely used as a flame retardant in many products like electronic equipments, plastics, furniture and textiles. BDE-209, a thyroid hormones (THs)-disrupting chemical, affects male reproductive health through altered THs status in mouse model. The present study was designed in continuation to our earlier work to elucidate whether early life exposure to BDE-209 has a long term potential risk to male reproductive health. This study, therefore, aimed to evaluate the effect of maternal BDE-209 exposure during lactation and to elucidate possible mechanism(s) of its action on male reproduction in adult Parkes mice offspring. Lactating female Parkes mice were orally gavaged with 500, and 700 mg/kg body weight of BDE-209 in corn oil from postnatal day (PND) 1 to PND 28 along with 6-propyl-2-thiouracil (PTU)-treated positive controls and vehicle-treated controls. Male pups of lactating dams were euthanized at PND 75. Maternal BDE-209 exposure during lactation markedly affected histoarchitecture of testis and testosterone production with concomitant down-regulation in the expression of various steroidogenic markers in adult offspring. Maternal exposure to BDE-209 during lactation also interfered with germ cell dynamics and oxidative status in testes of adult mice offspring. A decreased expression of connexin 43 and androgen receptor was also evident in testes of these mice offspring; further, number, motility and viability of spermatozoa were also adversely affected in these mice. The results thus provide evidences that maternal exposure to BDE-209 during lactation causes reproductive toxicity in adult mice offspring. � 2020 The AuthorsItem Role of reactive oxygen species in cancer progression: Molecular mechanisms and recent advancements(MDPI AG, 2019) Aggarwal V.; Tuli H.S.; Varol A.; Thakral F.; Yerer M.B.; Sak K.; Varol M.; Jain A.; Khan M.A.; Sethi G.Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies.Item Neuro-Protective Role Of Ginkgolide B In A?induced Neurodegeneration And Ache Enzyme Activity In Human Neuroblastoma Sh-Sy5Y Cells(Central University of Punjab, 2018) Mukherjee, Ankita; Mantha,Anil K.Ginkgolide B (GB) is being used as medicine in China for treating neurodegenerative diseases for a long time. Its neuroprotective role is getting well established. Alzheimer's disease (AD) is a neurodegenerative disease that has multiple factors associated with its onsetand is one of the most common causes of dementia in the world. GB is known to reduce the oxidative stress caused due to accumulation of amyloid beta (A?), a major hallmark of AD associated strongly with the production of oxidative stress via production of ROS. The increase in the expression of AChE has been reported and it has been associated with increased toxicity of A?. This study tried to decipher the relationship between A?, GB and AChE activity. In this study, it was found that A?(25-35)-induced oxidative stress leads to increased production of ROS and decreased AChE activity. On the other hand, GB decreased ROS production and expression of AChE, thus pointing toward its protective effect. GB increased the activity of AChE, suggesting that due to its antioxidant potentialit possibly caused a decrease in protein oxidation, and thus increased the activity of the AChE enzyme. Therefore, the results of the present study show the modulatory role of GB an AChE enzyme activity under oxidative stress conditions as seen in AD, suggesting the potential of GB in AD therapeutics