Mitochondrial transplantation against gentamicin-induced toxicity on rat renal proximal tubular cells: the higher activity of female rat mitochondria

Arjmand, Abdollah; Shiranirad, Saba; Ameritorzani, Fateme; Kamranfar, Farzaneh; Seydi, Enayatollah; Pourahmad, Jalal

doi:10.1007/s11626-022-00743-1

Cited by 5 publications

(2 citation statements)

References 47 publications

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“…The ndings of the mentioned studies are in line with our observations in the current work. In addition, several studies using cell models, similar to our work have proven the bene cial effects of mitochondrial transplantation to reduce drug-induced cell damages (21,41,42).…”

Section: Discussionsupporting

confidence: 71%

Transplantation of Healthy Mitochondria into Rat Renal Proximal Tubular Cells Reduces Colistin- Induced Mitochondrial Dysfunction and Cellular Damage: An In Vitro Study

Arjmand

Mohammadabadi

Faizi

et al. 2023

Preprint

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Background Kidney damage caused by colistin (polymyxin E) can bring about a decrease in creatinine clearance, potential proteinuria, cylindruria and oliguria in treated patients. It is therefore imperative to develop a new therapeutic strategy for reducing kidney damage after treatment with colistin. Mitochondrial damage is one of contributing factors in colistin-induced nephrotoxicity. Given the therapeutic benefits of mitochondrial transplantation by exogenous healthy mitochondria, we hypothesized that this strategy would be capable of ameliorating renal proximal tubular cells damage following exposure with colistin.Methods For this purpose, we isolated rat renal proximal tubular cells (RPTCs) form kidney and exposed them with toxic concertation of colistin with/without rat healthy isolated mitochondria for 4 hours. Cellular parameters such as lactate dehydrogenase (LDH), reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP), caspase 3 activation, lysosomal damage, glutathione and ATP content were measured.Results The results showed that administration of isolated mitochondria could improve colistin-induced nephrotoxicity and reduce mitochondrial dysfunction. Exogenous mitochondria reduced the activity of LDH, production of ROS, ATP and GSH depletion, loss of MMP, lysosomal damages and cell death.Conclusion To the best of our knowledge, these results provide the first direct experimental evidence that mitochondrial transplantation is capable of ameliorating cellular damage following treatment with colistin. These findings support that mitochondrial transplantation can be a promising therapeutic strategy for colistin-associated mitochondrial dysfunction and kidney damage.

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Section: Discussionsupporting

confidence: 71%

Transplantation of Healthy Mitochondria into Rat Renal Proximal Tubular Cells Reduces Colistin- Induced Mitochondrial Dysfunction and Cellular Damage: An In Vitro Study

Arjmand

Mohammadabadi

Faizi

et al. 2023

Preprint

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“…53,54 Intraarterial injection of mitochondria in female Yorkshire pigs undergoing an IRI model conferred reduced measures of kidney injury. 55 Mitochondrial transplantation in male rats undergoing IRI 56 or gentamicin-induced toxicity 57 was protective; in the latter case, this protection was more pronounced when mitochondria were from females. Given the importance of gonadal hormones, it is noteworthy that estrogen receptors have been identified in mitochondria, 58,59 and mitochondrial energetics are altered by manipulation of estrogen levels.…”

Section: Sex Differences In Mitochondrial Biologymentioning

confidence: 95%

Sex and Gender Differences in AKI

Curtis

2023

Kidney360

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Sex differences in acute kidney injury (AKI) continue to be identified. Generally, women are protected from AKI when compared to men. Much of the protection exhibited in women is diminished after menopause. These sex and age effects have also been noted in animal models of AKI. Gonadal hormones, as modifiers of incidence, severity, and progression of AKI, have been offered as likely contributors to this sex and age effect. In animal models of AKI, estrogen and testosterone appear to modulate susceptibility. Questions remain however regarding cellular and molecular changes that are initiated by modulation of these hormones, as both estrogen and testosterone have effects across cell types that play a role in AKI. Although findings have largely been informed by studies in males, molecular pathways that are involved in the initiation and progression of AKI may be modulated by gonadal hormones. Compounding the hormone-receptor effects are developmental effects of sex chromosomal complement and epigenetic influences that may confer sex-based baseline differences in gene and protein expression, and gene dosage effects of X-inactivation and escape on molecular pathways. Elucidation of sex-based protection may afford a more complete view of AKI and potential therapeutic interventions. Further, the impact on susceptibility to AKI in transgender patients, who receive life-altering and essential gender-affirming hormone therapy, requires greater attention. In this review, several potential contributors to the sex differences observed in humans and animal models are discussed.

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Mitotherapy inhibits against tenofovir induced nephrotoxicity on rat renal proximal tubular cells

Hosseini,

Hassanbeigloo,

Abbasi

et al. 2024

Biochemistry and Biophysics Reports

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Mitochondrial transplantation against gentamicin-induced toxicity on rat renal proximal tubular cells: the higher activity of female rat mitochondria

Cited by 5 publications

References 47 publications

Transplantation of Healthy Mitochondria into Rat Renal Proximal Tubular Cells Reduces Colistin- Induced Mitochondrial Dysfunction and Cellular Damage: An In Vitro Study

Transplantation of Healthy Mitochondria into Rat Renal Proximal Tubular Cells Reduces Colistin- Induced Mitochondrial Dysfunction and Cellular Damage: An In Vitro Study

Sex and Gender Differences in AKI

Mitotherapy inhibits against tenofovir induced nephrotoxicity on rat renal proximal tubular cells

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