Effects of developmental exposures to Bisphenol-A and Bisphenol-S on hepatocellular function in male Long-Evans rats

Liu, Keyi; Kadannagari, Surekha; DeRuiter, Jack; Pathak, Suhrud; Abbott, Kodye L.; Salamat, Julia M.; Pondugula, Satyanarayana R.; Akingbemi, Benson T.; Dhanasekaran, Muralikrishnan

doi:10.1016/j.lfs.2023.121752

Cited by 4 publications

(11 citation statements)

References 41 publications

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“…Using a Protein Assay reagent kit (Thermo Scientific Pierce 660 nm, Pierce, Rockford, IL), the colorimetric procedure was used to assess the protein, the process, by which a particular dye‐metal complex binds to protein in an acidic environment alters the dye's maximum absorption wavelength (660 nm). Bovine serum albumin 22 was utilized for standardization 23,24 …”

Section: Methodsmentioning

confidence: 99%

“…Complex‐I (NADH dehydrogenase) in the mitochondria catalyzes the conversion of NADH oxidation to NAD+. A standard curve was obtained using NADH 23,25–27 …”

Section: Methodsmentioning

confidence: 99%

“…Complex‐IV (Cytochrome‐C oxidase) in the mitochondria initiates the oxidation of Cytochrome‐C. A standard curve was obtained using Cytochrome‐C 23,26 …”

Section: Methodsmentioning

confidence: 99%

“…ROS content was determined by detecting the conversion of nonfluorescent chloromethyl‐DCF‐DA (2′, 7‐dichlorofluorescindiacetate, DCF‐DA) to fluorescent DCF using an excitation wavelength of 492 nm and an emission wavelength of 527 nm. This was done using spectrofluorometry 23,25–28 …”

Section: Methodsmentioning

confidence: 99%

“…The colorimetric method using thiobarbituric acid was used to quantify the lipid peroxide content. The formed thiobarbituric acid reactive substances (TBARS) were measured using a plate reader at 532 nm 23,26,28 …”

Section: Methodsmentioning

confidence: 99%

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Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons

Desai,

Majrashi,

Pathak

et al. 2024

Cancer Reports

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BackgroundIatrogenesis is an inevitable global threat to healthcare that drastically increases morbidity and mortality. Cancer is a fatal pathological condition that affects people of different ages, sexes, and races around the world. In addition to the detrimental cancer pathology, one of the most common contraindications and challenges observed in cancer patients is severe adverse drug effects and hypersensitivity reactions induced by chemotherapy. Chemotherapy‐induced cognitive neurotoxicity is clinically referred to as Chemotherapy‐induced cognitive impairment (CICI), chemobrain, or chemofog. In addition to CICI, chemotherapy also causes neuropsychiatric issues, mental disorders, hyperarousal states, and movement disorders. A synergistic chemotherapy regimen of Doxorubicin (Anthracycline‐DOX) and Cyclophosphamide (Alkylating Cytophosphane‐CPS) is indicated for the management of various cancers (breast cancer, lymphoma, and leukemia). Nevertheless, there are limited research studies on Doxorubicin and Cyclophosphamide's pharmacodynamic and toxicological effects on dopaminergic neuronal function.AimThis study evaluated the dopaminergic neurotoxic effects of Doxorubicin and Cyclophosphamide.Methods and ResultsDoxorubicin and Cyclophosphamide were incubated with dopaminergic (N27) neurons. Neuronal viability was assessed using an MTT assay. The effect of Doxorubicin and Cyclophosphamide on various prooxidants, antioxidants, mitochondrial Complex‐I & IV activities, and BAX expression were evaluated by Spectroscopic, Fluorometric, and RT‐PCR methods, respectively. Prism‐V software (La Jolla, CA, USA) was used for statistical analysis. Chemotherapeutics dose‐dependently inhibited the proliferation of the dopaminergic neurons. The dopaminergic neurotoxic mechanism of Doxorubicin and Cyclophosphamide was attributed to a significant increase in prooxidants, a decrease in antioxidants, and augmented apoptosis without affecting mitochondrial function.ConclusionThis is one of the first reports that reveal Doxorubicin and Cyclophosphamide induce significant dopaminergic neurotoxicity. Thus, Chemotherapy‐induced adverse drug reaction issues substantially persist during and after treatment and sometimes never be completely resolved clinically. Consequently, failure to adopt adequate patient care measures for cancer patients treated with certain chemotherapeutics might substantially raise the incidence of numerous movement disorders.

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Section: Methodsmentioning

confidence: 99%

“…Complex‐I (NADH dehydrogenase) in the mitochondria catalyzes the conversion of NADH oxidation to NAD+. A standard curve was obtained using NADH 23,25–27 …”

Section: Methodsmentioning

confidence: 99%

“…Complex‐IV (Cytochrome‐C oxidase) in the mitochondria initiates the oxidation of Cytochrome‐C. A standard curve was obtained using Cytochrome‐C 23,26 …”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons

Desai,

Majrashi,

Pathak

et al. 2024

Cancer Reports

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Rats' testicular toxicity induced by bisphenol A is lessened by crocin via an antiapoptotic mechanism and bumped P-glycoprotein expression

El-Beshbishy,

Waggas,

Ali

2024

Toxicon

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Effects of Cannabidiol, ∆9-Tetrahydrocannabinol, and WIN 55-212-22 on the Viability of Canine and Human Non-Hodgkin Lymphoma Cell Lines

Omer,

Pathak,

Mansour

et al. 2024

Biomolecules

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In our previous study, we demonstrated the impact of overexpression of CB1 and CB2 cannabinoid receptors and the inhibitory effect of endocannabinoids (2-arachidonoylglycerol (2-AG) and Anandamide (AEA)) on canine (Canis lupus familiaris) and human (Homo sapiens) non-Hodgkin lymphoma (NHL) cell lines’ viability compared to cells treated with a vehicle. The purpose of this study was to demonstrate the anti-cancer effects of the phytocannabinoids, cannabidiol (CBD) and ∆9-tetrahydrocannabinol (THC), and the synthetic cannabinoid WIN 55-212-22 (WIN) in canine and human lymphoma cell lines and to compare their inhibitory effect to that of endocannabinoids. We used malignant canine B-cell lymphoma (BCL) (1771 and CLB-L1) and T-cell lymphoma (TCL) (CL-1) cell lines, and human BCL cell line (RAMOS). Our cell viability assay results demonstrated, compared to the controls, a biphasic effect (concentration range from 0.5 μM to 50 μM) with a significant reduction in cancer viability for both phytocannabinoids and the synthetic cannabinoid. However, the decrease in cell viability in the TCL CL-1 line was limited to CBD. The results of the biochemical analysis using the 1771 BCL cell line revealed a significant increase in markers of oxidative stress, inflammation, and apoptosis, and a decrease in markers of mitochondrial function in cells treated with the exogenous cannabinoids compared to the control. Based on the IC50 values, CBD was the most potent phytocannabinoid in reducing lymphoma cell viability in 1771, Ramos, and CL-1. Previously, we demonstrated the endocannabinoid AEA to be more potent than 2-AG. Our study suggests that future studies should use CBD and AEA for further cannabinoid testing as they might reduce tumor burden in malignant NHL of canines and humans.

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Effects of developmental exposures to Bisphenol-A and Bisphenol-S on hepatocellular function in male Long-Evans rats

Cited by 4 publications

References 41 publications

Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons

Evaluate the in vitro effect of anthracycline and alkylating cytophosphane chemotherapeutics on dopaminergic neurons

Rats' testicular toxicity induced by bisphenol A is lessened by crocin via an antiapoptotic mechanism and bumped P-glycoprotein expression

Effects of Cannabidiol, ∆9-Tetrahydrocannabinol, and WIN 55-212-22 on the Viability of Canine and Human Non-Hodgkin Lymphoma Cell Lines

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