Hair Dye Related Acute Kidney Injury – A Clinical and Experimental Study

Reddy, Yanala Sandeep; Nabi, Shaik Abbdul; Rao, Chippada Appa; Srilatha, Chinthamaneni; Yadla, Manjusha; Naveen, P; Kishore, C. Krishna; Sridhar, Anappindi Venkata Satya Surya Naga; Kumar, V Siva

doi:10.3109/0886022x.2012.687346

Cited by 5 publications

(14 citation statements)

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“…Animal experiments revealed that approximately one-third of colorants disappeared from the skin within weeks after tattooing [ 32 ]. Furthermore, acute and chronic PPD poisoning in humans has caused renal, hepatic, and cardiac complications [ 15 , 33 ]. Further assessment of the health risk of PPD is imperative due to its widespread application, despite the low risk from the use of commercialized PPD-contained products.…”

Section: Discussionmentioning

confidence: 99%

“…The highest PPD-derived radioactivity was present in the muscle, skin, and liver of rodents after exposure, while clearance of PPD-derived radioactivity was primarily through the urine (68-86%) and secondarily through the feces (10-19%) [ 34 ]. Previous studies demonstrated that PPD led to acute renal failure [ 15 ] and impaired urothelial cells through ROS-mediated apoptosis and autophagy formation [ 17 – 19 ]. Our data suggested that toxic metabolites from PPD might impair renal tubular cells by inhibiting water absorption, resulting in early stage diuresis and late-stage oliguria with damaged urothelial cells leading to frequent urination by undefined mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Intermittent exposure to low-concentration PPD could be equivalent to a single, higher-dose exposure [ 37 ]. Acute PPD intoxication by oxidative stress, a direct toxic effect, and lipid peroxidation-induced bladder injury [ 14 , 16 ], kidney injury [ 13 , 15 ], hematological alteration [ 38 ], and testicular injury [ 11 , 39 ] have been observed following sub-chronic topical application in rats. PPD can also induce systemic immunologic effects in several organs and tissues or induce local inflammation [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

“…The highest cumulative PPD penetration obtained was 4.47 g/cm 2 , which yielded a 0.052 mg/kg systemic exposure dose (close to 60 μg/kg) according to SCCNFP/0129/99. We used a chronic minimal dose of 60 μg/kg/day intraperitoneally for 4 weeks compared to a previous experimental study that used a single dose [ 15 ]. The rats were placed in R-2100 metabolic cages (Lab Products, Rockville, Maryland) the day before surgical procedures to evaluate the fecal and urinary amount and voiding frequency.…”

Section: Methodsmentioning

confidence: 99%

“…PPD can induce production of excess oxygen species (ROS) that impair keratinocytes, germ cells, urothelial cells, and kidney cells through oxidative stress [ 6 , 11 – 14 ]. Oral PPD induced acute kidney injury, including glomerular and tubulointerstitial pathological changes, at a sub-lethal (40 mg/kg once) or minimal (20 mg/kg once) dose in a rat model [ 15 ]. PPD can also increase expression of oncoprotein p53, cyclooxygenase 2, and autophagy stimulation in human uroepithelial cells [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

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Synthetic nickel-containing superoxide dismutase attenuates para-phenylenediamine-induced bladder dysfunction in rats

et al. 2017

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Para (p)-phenylenediamine and its toxic metabolites induce excess reactive oxygen species formation that results in bladder voiding dysfunction. We determined the effects of synthetic Ni-containing superoxide dismutase mimics and the role of oxidative stress in p-phenylenediamine-induced urinary bladder dysfunction. P-phenylenediamine (60 μg/kg/day) was intraperitoneally administered for 4 weeks to induce bladder injury in female Wistar rats. Synthetic Ni-containing superoxide dismutase mimics, WCT003 (1.5 mg/kg) and WCT006 (1.5 mg/kg), were then intraperitoneally administered for 2 weeks. Transcystometrograms were performed in urethane-anesthetized rats. The in vitro and in vivo reactive oxygen species levels and pathological changes in formalin-fixed bladder sections were evaluated. Western blotting and immunohistochemistry elucidated the pathophysiological mechanisms of oxidative stress-induced apoptosis, autophagy, and pyroptosis. P-phenylenediamine increased voiding frequency, blood and urinary bladder levels of reactive oxygen species, and neutrophil and mast cell infiltration. It also upregulated biomarkers of autophagy (LC3 II), apoptosis (poly (ADP-ribose) polymerase), and pyroptosis (Caspase 1). WCT003 and WCT006 ameliorated reactive oxygen species production, inflammation, apoptosis, autophagy, pyroptosis, and bladder hyperactivity. P-phenylenediamine increased oxidative stress, inflammatory leukocytosis, autophagy, apoptosis, and pyroptosis formation within the urinary bladder. Novel synthetic nickel-containing superoxide dismutase mimics relieved p-phenylenediamine-induced bladder inflammation and voiding dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Synthetic nickel-containing superoxide dismutase attenuates para-phenylenediamine-induced bladder dysfunction in rats

et al. 2017

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A mechanistic analysis of henna in G6PD deficiency patients

Saghi

Gao

Giampietro

et al. 2023

Toxicologie Analytique et Clinique

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Hair Dye Ingredients and Potential Health Risks from Exposure to Hair Dyeing

Michailidou

Gahlon

Zeng

2022

Chem. Res. Toxicol.

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Given the worldwide popularity of hair dyeing, there is an urgent need to understand the toxicities and risks associated with exposure to chemicals found in hair dye formulations. Hair dyes are categorized as oxidative and nonoxidative in terms of their chemical composition and ingredients. For several decades, the expert panel’s Cosmetic Ingredient Review (CIR) has assessed the safety of many of the chemicals used in hair dyes; however, a comprehensive review of hair dye ingredients and the risk of exposure to hair dyeing has not been documented. Herein, we review the safety of the various chemicals in oxidative and nonoxidative hair dyes, toxicities associated with hair dyeing, and the carcinogenic risks related to hair dyeing. While many compounds are considered safe for users at the concentrations in hair dyes, there are conflicting data about a large number of hair dye formulations. The CIR expert panel has ratified a number of coloring ingredients for hair dyes and banned a series of chemicals as carcinogenic to animals and unsafe for this application. The use of these chemicals as raw materials for producing hair dyes may result in the synthesis of other contaminants with potential toxicities and increased risk of carcinogenesis. It is an open question whether personal or occupational hair dyeing increases the risk of cancer; however, in specific subpopulations, a positive association between hair dye use and cancer occurrence has been reported. To address this question, a better understanding of the chemical and mechanistic basis of the reported toxicities of hair dye mixtures and individual hair dye ingredients is needed. It is anticipated that in-depth chemical and systems toxicology studies harnessing modern and emerging techniques can shed light on this public health concern in the future.

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Hair Dye Related Acute Kidney Injury – A Clinical and Experimental Study

Cited by 5 publications

References 3 publications

Synthetic nickel-containing superoxide dismutase attenuates para-phenylenediamine-induced bladder dysfunction in rats

Synthetic nickel-containing superoxide dismutase attenuates para-phenylenediamine-induced bladder dysfunction in rats

A mechanistic analysis of henna in G6PD deficiency patients

Hair Dye Ingredients and Potential Health Risks from Exposure to Hair Dyeing

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