Severe subacute exposure to aluminium chloride (AlCl3) impairs renal function and induces cortical tubular injury; however, the concomitant balance between injury and repair in tubular epithelia remains incompletely defined. Accordingly, we aimed to use a high-dose regimen of AlCl3 (100 mg·kg−1·day−1 for 30 days, oral gavage) as a standardised renal stressor in male Wistar rats to quantify shifts along the injury–repair balance in the renal cortex and to test whether L-carnitine (LC) pretreatment (200 mg·kg−1·day−1) can attenuate these shifts. Twenty rats were assigned to four groups: control, LC alone, AlCl3 alone, and LC followed 60 min later by AlCl3. On day 31, we assessed body-weight gain, renal functional markers, blinded cortical lesion scoring, quantitative histochemistry, and immunohistochemical profiling of cleaved caspase-3 (apoptotic signalling) and Ki-67 (proliferative engagement) within the same cortical compartment. AlCl3 exposure produced a severe renal stress phenotype compared with controls, reducing body-weight gain from 99.8 ± 8.6 to 24.0 ± 8.3 g and increasing serum urea and creatinine from 26.40 ± 3.21 to 48.60 ± 5.81 mg/dL and from 0.606 ± 0.063 to 0.956 ± 0.147 mg/dL, respectively. Cortical injury increased from 0 (0–0) in controls to 15 (15–15) after AlCl3 exposure. AlCl3 also reduced strong PAS area from 97.92 ± 1.10% to 52.37 ± 14.68% and protein optical density from 0.353 ± 0.020 to 0.269 ± 0.039, while increasing collagen area fraction from 6.92 ± 1.67% to 18.40 ± 3.02% and cleaved caspase-3 from 1.0 (1.0–2.0) to 12.0 (12.0–12.0). Ki-67 labelling declined from 17.80 ± 3.35% to 6.00 ± 1.58%, indicating suppressed proliferative engagement. Compared with AlCl3 alone, LC pretreatment showed partial protection, with higher body-weight gain (70.0 ± 15.6 g), lower serum urea and creatinine (21.40 ± 2.30 mg/dL and 0.580 ± 0.084 mg/dL), lower cortical injury burden 3 (3–4), greater strong PAS area (89.25 ± 2.67%), higher protein optical density (0.354 ± 0.012), lower collagen area fraction (12.26 ± 1.70%), lower cleaved caspase-3 4.0 (4.0–6.0), and higher Ki-67 labelling (10.60 ± 2.30%). Residual cortical injury, persistent collagen elevation, and incomplete Ki-67 preservation indicate that LC pretreatment attenuated, but did not fully prevent, AlCl3-induced renal cortical alterations. Overall, high-burden AlCl3 exposure not only enhanced cell loss but also impaired regenerative renewal, whereas LC pretreatment partially preserved this injury–repair balance.
Abo-Zeid et al. (Thu,) studied this question.