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The polycystic ovarian syndrome is the utmost common endocrinopathy state in women. It is related to both reproductive and metabolic disorders. The MTHFR gene associated with the ovarian follicular action encodes the 5-MTHFR (methylenetetrahydrofolate reductase) enzyme, tangled in folate metabolism. MTHFR gene C677T polymorphism declines the enzyme activity and thus folate deficit and increases the level of homocysteine, which affects the progress of oocytes. Here, we evaluated the association of MTHFR gene C677T polymorphism with Polycystic ovary syndrome (PCOS) in the South Indian cohort of women. About 129 PCOS women with following Rotterdam criteria and 90 women controls were studied. PCR-RFLP technique was carried out on all PCOS women in this study. Dissimilarities in hormone levels in PCOS patients were detected. MTHFR gene polymorphism CC, CT, TT genotype was found to be 74, 16, 9.30% in patients correspondingly. However, in controls, it was 44.4, 24, 31%, respectively. A substantial difference was detected in the genotype frequency distributions among the patients and controls. Also, allele frequency was shown as 82.95% C allele and 17.83% T allele and 56.67%, 43.33% for C, and T allele in controls correspondingly. Our results indicate a possible association and suggest that MTHFR C677T polymorphism can be used as a potential biomarker for PCOS progress in the South Indian women. [ABSTRACT FROM AUTHOR]

The inflammatory responses associated with polycystic ovary syndrome (PCOS) may play a significant role in the severity of the disease. Emerging evidence report states that the polyunsaturated fatty acids are capable of ameliorating the PCOS condition. The therapeutic effects of γ-linolenic acid (GLA), an omega-6 fatty acid, in various inflammatory diseases have been reported. Yet, its role in PCOS associated inflammatory response remains unexplored. The aim of the study was to decipher the effects of GLA in PCOS and its role in the PPAR-γ pathway. In our study, female Wistar rats were stimulated with daily subcutaneous injections of DHEA (60 mg/kg per day) for 28 days to induce PCOS. Daily doses of GLA(10, 20, and 50 mg/kg) and Pioglitazone (P)(30 mg/kg) were administered orally for 14 days after PCOS induction. The levels of DHEA, leptin, PPAR-γ were measured by ELISA. The gene expression levels of leptin, TNF-α, IL-33, PPAR-γ, C/EBP-β, SREBP-1were determined by Real Time-PCR. We observed that the GLA significantly attenuated the DHEA and leptin levels. GLA treatment also upregulated PPAR-γ expression, when compared to the DHEA group. Further, GLA treatment showed a significant reduction in DHEA induced TNF-α, IL-33, C/EBP-β, and SREBP-1 levels in Wistar rat polycystic ovary tissue samples. The present findings could indicate that GLA is able to reduce the inflammatory response due to DHEA stimulation and thereafter potentially attenuate PCOS via the PPAR-γ pathway., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest., (Copyright © 2020 Society for Biology of Reproduction & the Institute of Animal Reproduction and Food Research of Polish Academy of Sciences in Olsztyn. Published by Elsevier B.V. All rights reserved.)

Human coronaviruses, especially COVID-19, is an emerging pandemic infectious disease with high morbidity and mortality. Coronaviruses are associated with comorbidities, along with the symptoms of it. SARS-CoV-2 is one of the highly pathogenic coronaviruses that causes a high death rate compared to the SARS-CoV and MERS. In this review, we focused on the mechanism of coronavirus with comorbidities and impairment in multi-organ function. The main dysfunction upon coronavirus infection is damage to alveolar and acute respiratory failure. It is associated with the other organ damage such as cardiovascular risk via an increased level of hypertension through ACE2, gastrointestinal dysfunction, chronic kidney disease, diabetes mellitus, liver dysfunction, lung injury, CNS risk, ocular risks such as chemosis, conjunctivitis, and conjunctival hyperemia, cancer risk, venous thromboembolism, tuberculosis, aging, and cardiovascular dysfunction and reproductive risk. Along with this, we have discussed the immunopathology and coronaviruses at a molecular level and therapeutic approaches for the coronavirus infection. The comorbidities and multi-organ failure of COVID-19 have been explained at a molecular level along with the base of the SARS-CoV and MERS-CoV. This review would help us to understand the comorbidities associated with the coronaviruses with multi-organ damage., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Chemotherapeutic antibiotic doxorubicin belongs to the anthracycline class, slaughters not only the cancer cells but also non-cancerous cells even in the non-targeted organs thereby resulting in the toxicity. The liver is primarily involved in the process of detoxification and this mini-review we focused mainly to investigate the molecular mechanisms heading hepatotoxicity caused due to doxorubicin administration. The alterations in the doxorubicin treated liver tissue include vacuolation of hepatocytes, degeneration of hepatocyte cords, bile duct hyperplasia and focal necrosis. About the literature conducted, hepatotoxicity caused by doxorubicin has been explained by estimating the levels of liver serum biomarkers, ROS production, antioxidant enzymes, lipid peroxidation, and mitochondrial dysfunction. The liver serum biomarkers such as ALT and AST, elated levels of free radicals inducing oxidative stress characterized by a surge in Nrf-2, FOXO-1 and HO-1 genes and diminution of anti-oxidant activity characterized by a decline in SOD, GPx, and CAT genes. The augmented levels of SGOT, SGPT, LDH, creatine kinase, direct and total bilirubin levels also reveal the toxicity in the hepatic tissue due to doxorubicin treatment. The molecular insight of hepatotoxicity is mainly due to the production of ROS, ameliorated oxidative stress and inflammation, deteriorated mitochondrial production and functioning, and enhanced apoptosis. Certain substances such as extracts from medicinal plants, natural products, and chemical substances have been shown to produce an alleviating effect against the doxorubicin-induced hepatotoxicity are also discussed., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Doxorubicin is an extensively applied anti-cancerous drug since 1950's and its usage is constrained because of its accumulation in a non-cancerous organ. Many studies have proven that doxorubicin causes reproductive toxicity depends on its dosage, particularly due to increased oxidative stress and apoptosis. A number of the researches have been carried out concerning its prevention. But there is a need to recognize the mechanism at the back of its toxicity to get better and improved method of treatment. To clarify the feasible mechanism of doxorubicin-mediated reproductive toxicity in rats, we have administrated doxorubicin at distinct dosages inclusive of low dosage (male rats that are at 230-250 g acquired cumulatively 1.5 mg/kg; ip; once per week for five weeks) and high dosage (male rats which are at 230-250 grams obtained cumulatively 15 mg/kg; ip; once every week for five weeks). Doxorubicin decreases antioxidant level such as GSH, Cu/Zn SOD, Mn SOD both in serum and testes. Increased oxidative stress is considered via elevated MDA level both in serum and testes. The level of ROS is measured via the DCFDA method in testes. Apoptosis become found through DNA fragmentation assay and quantification of Caspase 3, Caspase 9, Bcl2 and Cytochrome C. Doxorubicin mediated oxidative stress and apoptosis in testicular milieu is through deregulation of Nrf2, PGC-1α, AHR, ARNT, PXR, SUMO-1, UCP2, UCP3, ANX A5, Caspase 3, Caspase 9, Bcl2, Cytochrome C, GR, and GPX. In end, doxorubicin-mediated oxidative stress and apoptosis is through diverse transcriptional factors and genes with respect to decreased antioxidant level, augmented ROS level and Annexin A5 in the testicular milieu., (Copyright © 2019 Society for Biology of Reproduction & the Institute of Animal Reproduction and Food Research of Polish Academy of Sciences in Olsztyn. Published by Elsevier B.V. All rights reserved.)