Changes of antioxidant enzyme activity and heat shock protein content in lymphocytes of children with asthma

Perisic, Tatjana; Srećković, Miodrag; Matić, Gordana

doi:10.2298/abs0704257p

Cited by 4 publications

(3 citation statements)

References 25 publications

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“…Additional studies have shown the up-regulation of Hsp90 and Hsp72 in response to ROS-induced asthma attacks in young children. Even though the exact functions of Hsp90 and Hsp72 remain unknown, it has been suggested that the elevated levels of these heat shock proteins could be to refold denatured proteins that may result from ROS induced-oxidative stress [ 107 ], thereby preventing protein aggregates, cellular deteriorations, and further complications. Tong and Luo showed that elevated Hsp70 levels in peripheral blood mononuclear cells (PBMCs) suggest Hsp involvement in the pathogenesis of asthma infection [ 108 ].…”

Section: Hsps In Human Inflammatory Diseases (Hids) and Cancermentioning

confidence: 99%

Roles of Heat Shock Proteins in Apoptosis, Oxidative Stress, Human Inflammatory Diseases, and Cancer

et al. 2017

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Heat shock proteins (HSPs) play cytoprotective activities under pathological conditions through the initiation of protein folding, repair, refolding of misfolded peptides, and possible degradation of irreparable proteins. Excessive apoptosis, resulting from increased reactive oxygen species (ROS) cellular levels and subsequent amplified inflammatory reactions, is well known in the pathogenesis and progression of several human inflammatory diseases (HIDs) and cancer. Under normal physiological conditions, ROS levels and inflammatory reactions are kept in check for the cellular benefits of fighting off infectious agents through antioxidant mechanisms; however, this balance can be disrupted under pathological conditions, thus leading to oxidative stress and massive cellular destruction. Therefore, it becomes apparent that the interplay between oxidant-apoptosis-inflammation is critical in the dysfunction of the antioxidant system and, most importantly, in the progression of HIDs. Hence, there is a need to maintain careful balance between the oxidant-antioxidant inflammatory status in the human body. HSPs are known to modulate the effects of inflammation cascades leading to the endogenous generation of ROS and intrinsic apoptosis through inhibition of pro-inflammatory factors, thereby playing crucial roles in the pathogenesis of HIDs and cancer. We propose that careful induction of HSPs in HIDs and cancer, especially prior to inflammation, will provide good therapeutics in the management and treatment of HIDs and cancer.

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Section: Hsps In Human Inflammatory Diseases (Hids) and Cancermentioning

confidence: 99%

Roles of Heat Shock Proteins in Apoptosis, Oxidative Stress, Human Inflammatory Diseases, and Cancer

et al. 2017

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“…Moreover, Hsp90 expression in acetaminophen-treated mice was higher in the serum and liver samples ( Wu et al, 2017 ). The elevated levels of these heat shock proteins could refold denatured proteins resulted from ROS-induced-oxidative stress ( PeRIšIć et al, 2007 ). Of note, Farag et al (2015) reported increased oxidative stress indicators in the liver BLD-injected rabbits.…”

Section: Discussionmentioning

confidence: 99%

Boldenone Undecylenate-Mediated Hepatorenal Impairment by Oxidative Damage and Dysregulation of Heat Shock Protein 90 and Androgen Receptors Expressions: Vitamin C Preventive Role

Behairy¹,

Mohamed²,

Ebraheim³

et al. 2021

Front. Pharmacol.

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Boldenone Undecylenate (BLD) is a synthetic derivative of testosterone and a widely used anabolic androgenic steroid. The health risk of BLD use as a pharmaceutical or dietary supplement is still underestimated and under-reported. Vitamin C (VC) has been recognized as an antioxidant with prominent hepatorenal protective effects. This study investigated the possible preventive activity of VC against BLD-induced hepatorenal damage. Forty adult male Wistar rats were classified into five groups: control, vehicle control, VC (orally given 120 mg/kg b. wt./day), BLD (intramuscularly injected 5 mg/kg b. wt./week), and BLD + VC-treated groups. The experiment continued for eight weeks. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured. Serum contents of total protein (TP), albumin (ALB), globulin, total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and very-low-density lipoprotein–cholesterol (VLDL-C) were also assayed. Urea, creatinine, and uric acid levels were determined together with sodium and potassium electrolytes measuring. Moreover, oxidative stress indicators including reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GSR) as well as malondialdehyde (MDA) levels were measured in both hepatic and renal tissues. Corresponding histological examination of renal and hepatic tissues was conducted. Besides, immunohistochemical evaluations for androgen receptors protein (AR) and heat shock protein 90 (Hsp 90) expressions were performed. BLD caused significant rises in serum ALT, AST, TP, ALB, TC, TG, LDL-C, VLDL-C, urea, creatinine, uric acid, potassium, and MDA levels. Further, BLD-injected rats showed significant declines in the serum levels of HDL-C, sodium, GSH, GPx, GST, and GSR. Besides, distinct histopathological perturbations were detected in renal and hepatic tissues of BLD-injected rats. AR and Hsp 90 immunoexpression were increased in hepatic and renal tissues. In contrast, VC significantly reversed the BLD-induced hepatorenal damage in co-treated rats but not ameliorated AR protein overexpression. VC could be an efficient preventive supplement for mitigating BLD-induced hepatorenal damage, possibly via controlling oxidative stress events.

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“…Similarly, it is well established that polyunsaturated fatty acids (PUFA) are more susceptible to oxidative attack than either monounsaturated or saturated fatty acids, and there is evidence in mammals that long-lived species frequently have lower levels of PUFA in their cell membranes than short-lived species (Pamplona et al 1999). Furthermore, MacRae et al (2015) showed that humans and naked mole rats, with maximum lifespans of 120 and 30 years, respectively, exhibited higher expression of DNA repair genes than mice, and Salway et al (2011) showed a significant correlation between expression of heat shock proteins (HSPs) and maximum lifespan among 13 mammalian and avian species, reflecting that HSPs have been shown to refold denatured proteins resulting from oxidative damage (Perišić et al 2007).…”

Section: Introductionmentioning

confidence: 99%

The evolution of life history strategies in plants and its relationship to the evolution of protective cellular mechanisms against reactive oxygen species

Zakhary

Nagarajan

Ngô

et al. 2021

Preprint

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Purpose. The Oxidative Stress Theory of Aging (OSTA) states that accumulation of oxidative damage is a major contributor to aging; however, until now, no studies have examined whether perennial plants exhibit cellular mechanisms to better protect themselves against oxidative damage than annual plants, nor how these mechanisms may have evolved. Methods. We undertook three approaches to evaluate the capacity for annual and perennial plants to resist oxidative damage. The first approach involved using an electrolyte leakage assay to assess the rate of cellular damage in leaves exposed to exogenous H 2 O 2 . The second approach involved determining the concentration of exogenous H 2 O 2 required to maximize germination rates, which provides insight about the antioxidant levels in seeds. The third approach involved assessing the susceptibility of chlorophyll a and chlorophyll b to exogenous H 2 O 2 and determining chlorophyll a/b ratios. We also conducted an ancestral state reconstruction of life history strategies in order to interpret our results in an evolutionary context. Results. Leaves from deciduous and evergreen perennials showed a lower rate of cellular damage than leaves from annuals when exposed to exogenous H 2 O 2 . Seeds from deciduous perennials—but not biennials or evergreen perennials—required a higher H 2 O 2 concentration to maximize germination rate compared to seeds from annuals, suggesting that seeds from deciduous perennials have higher antioxidant levels. Although chlorophyll b was found to be more susceptible to damage from exogenous H 2 O 2 , chlorophyll a/b ratios did not differ among life history strategies. Ancestral state reconstruction revealed that the ancestral plant was most likely an evergreen perennial. Conclusion. Our results showcase that resistance to oxidative stress is necessary for perennial plants to survive over multiple years. The mechanisms responsible for the increased tolerance of perennial species to oxidative stress has not been fully elucidated by this study, but it does not involve changes to chlorophyll a/b ratios, as such changes could disrupt photosynthesis. The developmental onset of these protective mechanisms was delayed in evergreen perennials compared to deciduous perennials, perhaps because the ancestral evergreens were primarily focused on rapid colonization of the terrestrial environment, which requires faster germination rates induced by higher H 2 O 2 levels.

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Changes of antioxidant enzyme activity and heat shock protein content in lymphocytes of children with asthma

Cited by 4 publications

References 25 publications

Roles of Heat Shock Proteins in Apoptosis, Oxidative Stress, Human Inflammatory Diseases, and Cancer

Roles of Heat Shock Proteins in Apoptosis, Oxidative Stress, Human Inflammatory Diseases, and Cancer

Boldenone Undecylenate-Mediated Hepatorenal Impairment by Oxidative Damage and Dysregulation of Heat Shock Protein 90 and Androgen Receptors Expressions: Vitamin C Preventive Role

The evolution of life history strategies in plants and its relationship to the evolution of protective cellular mechanisms against reactive oxygen species

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