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Okra (Abelmoschus esculentus L.) is the most consumed vegetable worldwide with the potential for diverse ecological adaptation. However, increasing salinization and changing climatic conditions are posing serious threats to the growth, yield, and quality of okra. Therefore, to mitigate increasing soil salinization and ensure sustainable okra production under rapidly changing climatic conditions, evaluation of new okra germplasm to develop salt tolerant cultivars is direly needed. The present study was designed to evaluate the genetic resources of okra genotypes for salt tolerance at growth and reproductive phases. Based on mophological and physio-biochemical responses of plants under stress condition, genotypes were divided into salt tolerant and succeptible groups. The experiment was comprised of 100 okra genotypes and each genotype was grown under control conditions and 6.5 dS m -1 NaCl concentration in a pot having 10 kg capacity. The experiment was conducted in a completely randomized design and each treatment was replicated three times. The results showed vast genetic variability among the evaluated okra germplasm traits like days to emergence, pod length, pod diameter, plant height, stem girth, and other yield-related parameters. Correlation analysis showed a highly significant positive association among the number of leaves at first flower and plant height at first flower.Likewise, pod weight also revealed a highly significant positive relationship for pod weight plant -1 , pod length, and K + : Na + . Principal Component Analysis (PCA) revealed that out of 16 principal components (PCs), five components showed more than one eigenvalue and the first six PCs contributed 67.2% of the variation. Bi-plot analysis illustrated that genotypes 95, 111, 133, 99, and 128, under salt stress conditions, exhibited both high yield per plant and salt-tolerant behavior in other yield-related traits. On the basis of all studied traits, a salt susceptible group and a salt-tolerant group were formed. The salt tolerant group comprised of 97, 68, 95, 114, 64, 99, 111, 133, 128, and 109 genotypes, whereas, the salt susceptible group contained 137, 139, 130, 94, and 125 genotypes. Salt-tolerant okra genotypes were suggested to be used in further breeding programs aimed to develop salt tolerance in okra. These insights will empower precision breeding, underscore the importance of genetic diversity, and bear the potential to address the challenges of salt-affected soils while promoting broader agricultural resilience, economic prosperity, and food security., (© 2023. The Author(s).)

Diabetes is a complex metabolic disorder and different environmental toxicants including heavy metals have been involved in diabetes induction. Therefore, assessment of the environmental risk factors and heavy metals induced toxicity have become critical for reducing the consequences of metals pollutants. Previously, we reported heavy metals induced nephrotoxicity in non-diabetic and diabetic rats. Here, we extended our analysis by examining the heavy metals induced organs (heart, kidney, liver, pancreas, and spleen) damage in diabetic and non-diabetic Wistar rats using histopathology and quantitative real-time PCR (qRT-PCR). Following the generation of the diabetic rat model, the animals were exposed to heavy metals including lead (Pb), arsenic (As), manganese (Mn) and cadmium (Cd). Both non-diabetic and diabetic rats were exposed to heavy metals for 30 days and subsequently, the heart, kidney, liver, pancreas and spleen tissues were examined. Heavy metal treatment resulted in irregularly arranged myofibrils and vacuolization in the heart tissue of metal treated groups as evident from hematoxylin and eosin (H & E) staining. The kidney tissue of rats treated with heavy metals showed tubular degeneration, fibrosis, hemorrhage, and vacuolation. The liver of the heavy metals treated rats exhibited cellular degeneration and necrosis. The pancreatic tissue of streptozotocin injected untreated and metal treated rats revealed severe degeneration, necrosis, degranulation, shrinkage, and depression in the islets of Langerhans. Increased red pulp area and congestion were observed in the spleen of the metal mixture treated non-diabetic and diabetic rats. In line with the histological data, the qRT-PCR analysis showed downregulated expression of Bcl 2 and upregulation of Caspase-3 in non-diabetic and diabetic metal treated rats as compared to the non-diabetic untreated rats. In conclusion, the present study revealed, diabetic rats are more prone to metal alone as well as metal mixture induced organ damage as compared to non-diabetic rats.

Cisplatin is an extensively used chemotherapeutic drug for lung cancer, but the development of resistance decreases its effectiveness in the treatments of non-small cell lung cancer (NSCLC). In this study, we examined the effects of metformin, a widely used antidiabetic drug, on cisplatin radiosensitization in NSCLC cell lines. Human NSCLC cell lines, A549 (cisplatin-resistant) and H460 (cisplatin-sensitive), were treated with metformin, cisplatin or a combination of both drugs before ionizing radiation. Cell proliferation, clonogenic assays, western blotting, cisplatin-DNA adduct formation and immunocytochemistry were used to characterize the treatments effects. Metformin increased the radiosensitivity of NSCLC cells. Metformin showed additive and over-additive effects in combination with cisplatin and the radiation response in the clonogenic assay in H460 and A549 cell lines (p = 0.018 for the interaction effect between cisplatin and metformin), respectively. At the molecular level, metformin led to a significant increase in cisplatin-DNA adduct formation compared with cisplatin alone (p < 0.01, ANOVA-F test). This was accompanied by a decreased expression of the excision repair cross-complementation 1 expression (ERCC1), a key enzyme in nucleotide excision repair pathway. Furthermore, compared with each treatment alone metformin in combination with cisplatin yielded the lowest level of radiation-induced Rad51 foci, an essential protein of homologous recombination repair. Ionizing radiation-induced γ-H2AX and 53BP1 foci persisted longer in both cell lines in the presence of metformin. Pharmacological inhibition of AMP-activated protein kinase (AMPK) demonstrated that metformin enhances the radiosensitizing effect of cisplatin through an AMPK-dependent pathway only in H460 but not in A549 cells. Our results suggest that metformin can enhance the effect of combined cisplatin and radiotherapy in NSCLC and can sensitize these cells to radiation that are not sensitized by cisplatin alone.

Epidermal growth factor receptor (EGFR) tyrosine kinase is commonly overexpressed in human cancers; however, the cellular mechanisms regulating EGFR expression remain unclear. p53, p63 and p73 are transcription factors regulating many cellular targets involved in controlling the cell cycle and apoptosis. p53 activates EGFR expression, whereas TAp63 represses EGFR transcription. The involvement of p73 in the regulation of EGFR has not been reported. Here, a strong correlation between EGFR overexpression and increased levels of the oncogenic DeltaNp73 isoform in head and neck squamous cell carcinoma (HNSCC) cell lines was observed. Ectopic expression of TAp73, particularly TAp73beta, resulted in suppression of the EGFR promoter, significant downregulation of EGFR protein and efficient induction of cell death in all six EGFR-overexpressing HNSCC cell lines. EGFR overexpression from a heterologous LTR promoter protected lung cancer cells from TAp73beta-induced EGFR suppression and apoptosis. Expression of TAp73beta efficiently induced promyelocytic leukaemia (PML) protein expression and PML knockdown by shRNA attenuated the downregulation of EGFR and induction of apoptosis by p73 in HNSCC cells. Furthermore, PML was found to be important for E1A-induced suppression of EGFR and subsequent killing of HNSCC cells. Our data therefore suggest a novel pathway involving PML and p73 in the regulation of EGFR expression.