Acute exposure to mercury chloride (HgCl₂) causes acute kidney injury (AKI). Some metals interfere with protein folding, leading to endoplasmic reticulum stress (ERS), and the activation of cell death mechanisms, but in the case of mercury, there is no knowledge about whether the ERS mediates tubular damage. This study aimed to determinate if HgCl₂ causes an AKI course with temporary activation of ERS and if this mechanism is involved in kidney cell death. Male mice were intoxicated with 5 mg/kg HgCl₂ and sacrificed after 24, 48, 72, and 96 h of mercury administration. The kidneys of euthanized mice were used to assess the renal function, oxidative stress, redox environment, antioxidant enzymatic system, cell death, and reticulum stress markers (PERK, ATF-6, and IRE1α pathways). The results indicate temporary-dependent renal dysfunction, oxidative stress, and an increase of glutathione-dependent enzymes involved in the bioaccumulation process of mercury, as well as the enhancement of caspase 3 activity along with IRE1a, GADD-153, and caspase 12 expressions. Mercury activates the PERK/eIF2α branch during the first 48 h. Meanwhile, the activation of PERK/ATF-4 branch allowed for ATF-4, ATF-6, and IRE1α pathways to enhance GADD-153. It led to the activation of caspases 12 and 3, which mediated the deaths of the tubular and glomerular cells. This study revealed temporary-dependent ERS present during AKI caused by HgCl₂, as well as how it plays a pivotal role in kidney cell damage.

In this study, the effects of the supplementation of natural and synthetic antioxidant additives in layer diets on egg weight loss, yolk lipid peroxidation (TBARS values) and fatty acid composition of eggs stored at different temperatures and duration were evaluated. In total, 112 48- weeks-old Bovans White layers were randomly allotted to four dietary treatments with four replicates of seven birds each. The treatments consisted of a control diet, containing no additives, and diets with the inclusion of 200 mg synthetic vitamin E/kg, 1000 mg thyme extract/kg and 1000 mg rosemary extract/kg. Dietary treatments did not influence (p>0.05) relative weight loss of eggs stored for 14, 28, and 56 days, except for those from rosemary-fed hens stored at room temperature on d 42, which were significantly lighter than the eggs from vitamin E- and thyme-fed hens (p<0.001). Relative egg weight loss was significantly higher (p<0.001) when stored at room temperature than under refrigeration, independently of storage time. In eggs stored at room temperature, yolk TBARS values were significantly lower (p<0.001) in the eggs of vitamin E-fed hens, whereas no influence (p>0.05) of dietary treatment on yolk TBARS values were detected in refrigerated eggs. The inclusion of the synthetic and both natural antioxidants in layer diets significantly reduced stearic acid (C18: 0) level in the egg yolk. In addition, only natural antioxidants significantly increased yolk levels of palmitoleic acid (C16: 1) and vaccenic acid (C18: 1n7). The results of the present study showed that adequate storage temperature was more effective in improving egg shelf life than feeding layers synthetic or natural antioxidant additives. However, the positive effects of the evaluated natural antioxidants on yolk fatty acid composition suggest their supplementation to layer diets may provide health benefits to the consumer.

Prostate cancer is a significant global health concern that requires innovative therapeutic investigations. Here, the potential anticancer properties of tannic acid were evaluated by examining its effects on apoptosis in prostate cancer cell lines. PC-3 and LnCaP prostate adeno carcinoma cells, along with PNT1A prostate control cells, were cultured and divided into untreated and tannic acid-treated groups. Cell proliferation, cytotoxicity, and effects of tannic acid on the cell death mechanism were evaluated. mRNA expression levels of 84 genes were explored in cells following tannic acid treatment. Notably, tannic acid-induced down-regulation of several pro-survival genes, including ATM, BCL2, BCL2A1, BIK, BIRC2, BIRC3, BRE, CASP3, CASP6, CASP8, CHEK2, CRADD, PPIA, RPA3, TNFSF18, TRAF1, TRAF2, TRAF4, and TRAF5 in both cell lines. Moreover, tannic acid treatment led to the up-regulation of various pro-apoptotic genes, such as BCL10, BIRC3, BNIP3, CASP1, CASP5, CD40, CIDEB, DAPK2, FASLG, GADD45A, MYD88, RPA 3, TNFRSF10D, TNFRSF17, TNFRSF8, TNFSF13B, TNFSF4, TNFSF7, TNFSF8, TNFSF9, TP53, TRAF1, and TRAF2 in both PC-3 and LnCap cells. These findings highlight tannic acid’s ability to induce apoptosis in prostate cancer cells through pro-apoptotic pathways. This study concludes that tannic acid selectively inhibits prostate cancer cell growth.

In the Bulgarian aquaculture sector, focusing research efforts on the technical specifications of the cultivation of African catfish (Clarias gariepinus) is important due to the need for more information. We aimed to assess the impact of light intensities on prolactin and cortisol levels as stress markers in African catfish. Fish were acclimated over an appropriate period to the short photoperiod (16D and 8L) and then distributed randomly to three groups, each separated by sex. Fish exposed to different light intensities (63, 51, and 40 lux, respectively) were followed for 45 days by lux meter. Blood samples were collected from the caudal vein using a 2 ml K2EDTA-coated syringe. A laser fluorescence reader assayed plasma prolactin and cortisol. The pituitary was removed from anesthetized fish and fixed for histological examinations. The results of our study suggest that increasing light intensity increases prolactin and cortisol levels in African catfish.