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Abstract Beta vulgaris L. is a root vegetable that is consumed mainly as a food additive. This study aimed to describe the protective effect of B. vulgaris on Fe2+-mediated oxidative liver damage through in vitro, ex vivo, and in silico studies to establish a strong rationale for its protective effect. To induce oxidative damage, we incubated the livers of healthy male rats with 0.1 mM FeSO4 to induce oxidative injury and coincubated them with an aqueous extract of B. vulgaris root (BVFE) (15–240 µg/mL). Induction of liver damage significantly (p

Abstract Salmonella Typhi is a major global concern in many low- and middle-income countries. In addition, the emergence and persistence of drug resistant strains has increased the impact of this disease. Plant metabolites have been explored traditionally and scientifically as antimicrobial agents. Thus, this study was designed to investigate the antimicrobial potential of acetone leaf fractions of H. indica against S. Typhi. Dried pulverized leaves of H. indica were extracted using cold maceration with acetone after defatting with n-hexane. The leaf extract was concentrated and subjected to column chromatography and eight bioactive fractions were identified. The fractions were characterized using gas chromatography-mass spectrometry. The fractions were evaluated for antibacterial activity against Salmonella Typhi in-vitro and in-silico. The lowest MIC was observed in fractions 20 and 21 (0.375 mg/mL) while the lowest MBC was observed in all fractions except 7, 17 and 18 (0.375 mg/mL). A ligand from fraction 8 had the highest binding affinity to Type I dehydroquinase (-3.4) and a ligand from fraction 7 had the highest binding affinity to Gyrase B (-11.2). This study concludes that the overall antimicrobial activity of the acetone leaf extract of H. indica provided evidence that it contains drug-like compounds that can be further explored as a drug candidate against S. Typhi.

Infertility has become a significant health burden around the globe as it is believed that 15 % of married couples struggle with infertility, with half of the problem accrued to the male. The issue of male infertility could be traced to insufficient or absence of spermatozoa. Glucose metabolism is essential for continued spermatogenesis and for the reproductive potential of sperm cells. Appropriate nutrition is critical in maintaining reproductive function as caloric restriction along with weight reduction, excessive food consumption and obesity are harmful to reproductive function. The link between metabolism and reproduction is tied to metabolic hormones like insulin, leptin and thyroid, extracellular environment, mitochondria function, nutrient substrate, availability, and environmental stressors. Although matured spermatozoa utilize glucose directly, it is not the preferred energy substrate for germ cells as they rely on Sertoli cells to supply lactate. The reproductive potential of sperm cells depends on certain modifications like hyperactivated motility, which is mainly dependent on glucose metabolism. Without other energy sources, spermatozoa utilize their internal lipid stores. The uptake and metabolism of glucose by sperm are essential endpoints for determining the potential fertility of male individuals. The biological energy in sperm cells fuels all the physiological processes they engage in, from their deposition in the female reproductive tract to the point where they fertilize an egg. This article thus reviews facts pertinent to the energy metabolism of male germ cells and Sertoli cells.

The mitophagy process, a type of macroautophagy, is the targeted removal of mitochondria. It is a type of autophagy exclusive to mitochondria, as the process removes defective mitochondria one by one. Mitophagy serves as an additional level of quality control by using autophagy to remove superfluous mitochondria or mitochondria that are irreparably damaged. During spermatogenesis, mitophagy can influence cell homeostasis and participates in a variety of membrane trafficking activities. Crucially, it has been demonstrated that defective mitophagy can impede spermatogenesis. Despite an increasing amount of evidence suggesting that mitophagy and mitochondrial dynamics preserve the fundamental level of cellular homeostasis, little is known about their role in developmentally controlled metabolic transitions and differentiation. It has been observed that male infertility is a result of mitophagy's impact on sperm motility. Furthermore, certain proteins related to autophagy have been shown to be present in mammalian spermatozoa. The mitochondria are the only organelle in sperm that can produce reactive oxygen species and finally provide energy for sperm movement. Furthermore, studies have shown that inhibited autophagy-infected spermatozoa had reduced motility and increased amounts of phosphorylated PINK1, TOM20, caspase 3/7, and AMPK. Therefore, in terms of reproductive physiology, mitophagy is the removal of mitochondria derived from sperm and the following preservation of mitochondria that are exclusively maternal.