Acrylamide, one of the major environmental public health problems, results from its increased accumulation in the process of cooking food materials. This study aimed to demonstrate the light and electron microscopic structural effects of acrylamide on the skeletal muscle fibers of adult male albino rat tongue and to investigate the possible protective effect of vitamin E co-administration. Thirty adult male albino Sprague–Dawley rats were divided into 3 groups, each group included 10 rats. Group I (control), group II which was subdivided into two equal subgroups: subgroup IIa: included 5 rats that received acrylamide orally once daily for 20 days. Subgroup IIb: included 5 rats that received acrylamide orally once daily for 40 days. Group III was also subdivided into two equal subgroups: subgroup IIIa: included 5 rats that received acrylamide and vitamin E orally once daily for 20 days. Subgroup IIIb: included 5 rats that received acrylamide and vitamin E orally once daily for 40 days. At the end of the experiment the tongue was dissected out for histological and electron microscopic studies, another muscle sample was homogenized and processed for biochemical estimation of malondialdehyde (MDA) and total antioxidant capacity (TAC). Light microscopic study of tongue skeletal muscles in acrylamide exposed animals revealed abnormal wavy course and splitting of the muscle fibers with fatty infiltration in between. Moreover, pyknosis and remnants of nuclei were detected. EM revealed marked aggregation of mitochondria of different size and shape with giant cells formation, and partial loss of myofilaments. There were statistically significant increase in MDA and decrease in TAC indicating oxidative stress in acrylamide administrated groups (group II) than the control group which increased by prolonged duration (subgroup IIb versus subgroup IIa, p < 0.0001). This oxidative stress could explain the histological changes in tongue muscles of acrylamide exposed rats. Co-administration of vitamin E with acrylamide ameliorated most of the above mentioned histological changes in the animals used and signs of improvement that became better with prolonged administration of it (subgroup IIIb versus subgroup IIIa, p < 0.0001) were detected. It could be concluded that, chronic exposure to acrylamide might lead to skeletal muscle damage in rat tongue which becomes worth with prolonged duration of exposure. Acrylamide induced oxidative stress is the implicated mechanism of such histological changes. This toxic effect of acrylamide could be minimized when vitamin E is given concomitantly with it by its antioxidant effect.

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Cigarette smoking is harmful to the health of both smokers and nonsmokers. It is a major cause of death. This study aimed to investigate the structural changes in the zona fasciculata of albino rats caused by nicotine and the protective effect of grape seeds with or without the stoppage of nicotine administration. Thirty-five adult male rats were used and equally divided into five groups: negative and positive control groups (Groups I and II), nicotine-treated group (Group III), nicotine- and grape seed extract-treated group (Group IV), and nicotine withdrawal and grape seed extract-treated group (Group V). Adrenal glands were dissected and prepared for histological studies. The majority of zona fasciculata cells of Group III showed striking changes in terms of swelling of the cells with marked cytoplasmic vacuolation, many pyknotic nuclei, and increased immunoexpression to caspase 3 antibodies. By electron microscopy, a marked increase in lipid deposition with its appearance in the capillary between zona fasciculata cells was noticed. Heterochromatic nuclei and dilated smooth endoplasmic reticulum were noted. Degenerated mitochondria and some mitochondria that had cavitation with a progressive loss of their cristae were seen. The zona fasciculata cells of Group IV were partially improved, while in Group V, those cells showed complete improvement. We can conclude that nicotine causes severe histological changes in zona fasciculata cells. Grape seed extract can partially ameliorate these changes, and complete recovery is achieved with grape seed extract after the stoppage of nicotine administration.

The development of the field of nanotechnology has revolutionized various aspects in the fields of modern sciences. Nano-medicine is one of the primary fields for the application of nanotechnology techniques. The current study sheds light on the reno-protective impacts of gold nano-particles; nanoGold (AuNPs) against 5-flurouracil (5-FU)-induced renal toxicity. Indeed, the use of 5-FU has been associated with kidney injury which greatly curbs its therapeutic application. In the current study, 5-FU injection was associated with a significant escalation in the indices of renal injury, i.e., creatinine and urea. Alongside this, histopathological and ultra-histopathological changes confirmed the onset of renal injury. Both gene and/or protein expression of nuclear factor erythroid 2–related factor 2 (Nrf-2) and downstream antioxidant enzymes revealed consistent paralleled anomalies. AuNPs administration induced a significant renal protection on functional, biochemical, and structural levels. Renal expression of the major sensor of the cellular oxidative status Nrf-2 escalated with a paralleled reduction in the renal expression of the other contributor to this axis, known as Kelch-like ECH-associated protein 1 (Keap-1). On the level of the effector downstream targets, heme oxygenase 1 (HO-1) and gamma-glutamylcysteine synthetase (γ-GCS) AuNPs significantly restored their gene and protein expression. Additionally, combination of AuNPs with 5-FU showed better cytotoxic effect on MCF-7 cells compared to monotreatments. Thus, it can be inferred that AuNPs conferred reno-protective impact against 5-FU with an evident modulatory impact on Nrf-2/Keap-1 and its downstream effectors, HO-1 and γ-GCS, suggesting its potential use in 5-FU regimens to improve its therapeutic outcomes and minimize its underlying nephrotoxicity.

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Background: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. Methods: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. Results: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, α, and β cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. Conclusion: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of α-lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

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