Diverse Farming Systems and their Impact on Macro and Microelement Content of Vegetables & Crops.

BACKGROUND: The present study investigates the effect of conventional and organic farming systems on the nutritional profile of crops. Different crops, namely -millet, sorghum, sesame, mustard, fenugreek, berseem, pea, potato, and onion were cultivated through conventional agriculture in which chemical fertilizers like urea, DAP (Diammonium Phosphate) and pesticides were used and organic farming in which organic fertilizers like seaweed and vermicompost were used. OBJECTIVE: The experimental study was done on a field in north India from 2019 to 2021 in six different seasons, and the nutrient profile of the crops with respect to macroelements (S, K, Na, P, Ca, Mg) and microelements (B, Cu, Fe, Mn, Zn, Al) was compared. METHODS: Macro and microelements were analyzed by Element analyzer and ICP-OES in both types of farming systems. The content of macro, as well as microelements, was found to be significantly higher in all the organically produced crops as compared to the conventionally grown crops. RESULTS: Significant differences were observed in the macroelement content of organic onion (P- 900 mg/kg, K-2000mg/kg) and organic pea (K 2250 mg/kg) as compared to the content of conventionally grown onion (P-756 mg/kg, K- 1550 mg/kg) and pea (K-2000 mg/kg). Similarly, microelement content in the organic sesame (Fe - 3.12 mg/kg), organic millet (Fe- 2.19 mg/kg), and organic potato (Zn-200 mg/kg) was higher as compared to conventionally grown sesame (Fe 2.05 mg/kg), millet (Fe- 1.56 mg/kg) and potato (Zn 167 mg/kg). CONCLUSION: This investigation concludes that crops with optimum nutritional content can be produced through organic farming with minimum input and maximum production.

Therapeutic Targeting of Mitochondrial Plasticity and Redox Control to Overcome Cancer Chemoresistance.

Significance: Mitochondria are subcellular organelles performing essential metabolic functions contributing to cellular bioenergetics and regulation of cell growth or death. The basic mitochondrial function in fulfilling the need for cell growth and vitality is evidenced whereby cancer cells with depleted mitochondrial DNA (rho zero, p0 cells) no longer form tumors until newly recruited mitochondria are internalized into the rho zero cells. Herein lies the absolute dependency on mitochondria for tumor growth. Hence, mitochondria are key regulators of cell death (by apoptosis, necroptosis, or other forms of cell death) and are, therefore, important targets for anticancer therapy. Recent Advances: Mitochondrial plasticity regulating their state of fusion or fission is key to the chemoresistance properties of cancer cells by promoting pro-survival pathways, enabling the mitochondria to mitigate against the cellular stresses and extreme conditions within the tumor microenvironment caused by chemotherapy, hypoxia, or oxidative stress. Critical Issues: This review discusses many characteristics of mitochondria, the processes and pathways controlling the dynamic changes occurring in the morphology of mitochondria, the roles of reactive oxygen species, and their relationship with mitochondrial fission or fusion. It also examines the relationship of redox to mitophagy when mitochondria become compromised and its effect on cancer cell survival, stemness, and the changes accompanying malignant progression from primary tumors to metastatic disease. Future Directions: A challenging question that arises is whether the changes in mitochondrial dynamics and their regulation can provide opportunities for improving drug targeting during cancer treatment and enhancing survival outcomes. Antioxid. Redox Signal. 39, 591-619.

MicroRNAs as master regulators of FOXO transcription factors in cancer management.

MicroRNAs are critical regulators of the plethora of genes, including FOXO "forkhead" dependent transcription factors, which are bonafide tumour suppressors. The FOXO family members modulate a hub of cellular processes like apoptosis, cell cycle arrest, differentiation, ROS detoxification, and longevity. Aberrant expression of FOXOs in human cancers has been observed due to their down-regulation by diverse microRNAs, which are predominantly involved in tumour initiation, chemo-resistance and tumour progression. Chemo-resistance is a major obstacle in cancer treatment. Over 90% of casualties in cancer patients are reportedly associated with chemo-resistance. Here, we have primarily discussed the structure, functions of FOXO and also their post-translational modifications which influence the activities of these FOXO family members. Further, we have addressed the role of microRNAs in carcinogenesis by regulating the FOXOs at post-transcriptional level. Therefore, microRNAs-FOXO axis can be exploited as a novel cancer therapy. The administration of microRNA-based cancer therapy is likely to be beneficial to curb chemo-resistance in cancers.

Renal cell carcinoma management: A step to nano-chemoprevention.

Renal cell carcinoma (RCC) is one of the most common kidney cancers, responsible for nearly 90 % of all renal malignancies. Despite the availability of many treatment strategies, RCC still remains to be an incurable disease due to its resistivity towards conventional therapies. Nanotechnology is an emerging field of science that offers newer possibilities in therapeutics including cancer medicine, specifically by targeted delivery of anticancer drugs. Several phytochemicals are known for their anti-cancer properties and have been regarded as chemopreventive agents. However, the hydrophobic nature of many phytochemicals decreases its bioavailability and distribution, thus showing limited therapeutic effect. Application of nanotechnology to enhance chemoprevention is an effective strategy to increase the bioavailability of phytochemicals and thereby its therapeutic efficacy. The present review focuses on the utility of nanotechnology in RCC treatment and chemopreventive agents of RCC. We have also visualized the future prospects of nanomolecules in the prevention and cure of RCC.

Removal of propylene and butylene as individual compounds with compost and wood chip biofilters.

Propylene and butylene are highly reactive volatile organic compounds (HRVOCs) in terms of ground-level ozone formation. This study examined the effectiveness of biofiltration in removing propylene and butylene as separate compounds. Specific objectives were (1) to measure maximum removal efficiencies for propylene and butylene and the corresponding microbial acclimation times, which will be useful in the design of future biofilters for removal of these compounds; (2) to compare removal efficiencies of propylene and butylene for different ratios of compost/hard wood-chip media; and (3) to identify the microorganisms responsible for propylene and butylene degradation. Two laboratory-scale polyvinyl chloride biofilter columns were filled with 28 in. of biofilter media (compost/wood-chip mixtures of 80:20 and 50:50 ratios). Close to 100% removal efficiency was obtained for propylene for inlet concentrations ranging from 2.9 x 10(4) to 6.3 x 10(4) parts per million (ppm) (232-602 g/m3-hr) and for butylene for inlet concentrations ranging from 91 to 643 ppm (1.7-13.6 g/m3-hr). The microbial acclimation period to attain 100% removal efficiency was 12-13 weeks for both compounds. The lack of similar microbial species in the fresh and used media likely accounts for the long acclimation time required. Both ratios of compost/wood chips (80:20 and 50:50) gave similar results. During the testing, media pH increased slightly from 7.1 to 7.5-7.7. None of the species in the used media that treated butylene were the same as those in the used media that treated propylene, indicating that different microbes are adept at degrading the two compounds.

Nano-TiO2-induced apoptosis by oxidative stress-mediated DNA damage and activation of p53 in human embryonic kidney cells.

The aim of the present study is to explore the mechanism of cytotoxic and genotoxic effects of TiO(2) nanoparticles on human embryonic kidney (HEK-293) cells. Toxicity was evaluated using changes in various cellular parameters of HEK-293 cells like morphology, viability, metabolic activity, oxidative stress and apoptosis. Oxidative stress was measured by the level of reactive oxygen species (ROS), lipid peroxidation, superoxide dismutase, catalase and glutathione peroxidase. Apoptosis induced by nano-TiO(2) was characterized by PI staining and DNA ladder assay. Furthermore, apoptotic proteins such as p53 and Bax were analysed by western blot. Our results indicate that nano-TiO(2) induces cytotoxicity in a time- and dose-dependent manner. Oxidative stress and apoptosis were induced by exposure to nano-TiO(2). Moreover, the expression of p53, Bax and caspase-3 were increased in a dose-dependent pattern. In conclusion, ROS-mediated oxidative stress, the activation of p53, Bax, caspase-3 and oxidative DNA damage are involved in the mechanistic pathways of nano-TiO(2)-induced apoptosis in HEK-293 cells.

GSTP1 methylation and polymorphism increase the risk of breast cancer and the effects of diet and lifestyle in breast cancer patients.

Glutathione S-transferases (GSTs) are an important group of isoenzymes that play an essential role in the detoxification of carcinogens. Polymorphism at exon 5 of the GST π family decreases the catalytic activity and affects the detoxification ability of the enzyme, GSTP1. GSTP1 promoter hypermethylation and loss of expression are frequently observed in various types of carcinoma. We hypothesized that somatic epigenetic modification in homozygous mutants increases the degree to which breast cancer risk is affected by lifestyle factors and dietary habits. The present study used tumor biopsies and blood samples from 215 breast cancer patients and 215 blood samples from healthy donors. GSTP1 polymorphism was studied using PCR-restriction fragment length polymorphism, methylation using methylation-specific PCR and loss of expression using immunohistochemistry and western blotting. No significant increase was observed in the breast cancer risk of individuals with the mutant (Val) allele [odds ratio (OR), 1.48; 95% confidence interval (CI), 0.97-2.26 for heterozygotes; OR, 1.42; 95% CI, 0.86-2.42 homozygous mutants]. GSTP1 promoter hypermethylation was detected in one-third of tumor biopsies (74/215) and was found to be associated with a loss of expression. Genotype and tumor methylation associations were not observed. Estrogen (ER) and progesterone (PR) receptor-positive tumors had a higher methylation frequency. GSTP1 polymorphism was not associated with increased promoter hypermethylation. The results suggest that GSTP1 methylation is a major event in breast carcinogenesis and may act as a tumor-specific biomarker.