Subacute Exposure to Aldrin, Endosulfan and Lindane Differentially Alters Metabolic and Inflammatory Gene Expression in White and Brown Adipose Tissue of Male Rats


Boujanah N. A. M., Erdogan C. S., Sumer E., Yakin C., YILMAZ B.

Cell Biochemistry and Function, cilt.44, sa.7, 2026 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 44 Sayı: 7
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1002/cbf.70262
  • Dergi Adı: Cell Biochemistry and Function
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Academic Search Ultimate (EBSCO), Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO)
  • Anahtar Kelimeler: adipose tissue, aldrin, endosulfan, inflammation, lindane, obesogen
  • Dokuz Eylül Üniversitesi Adresli: Evet

Özet

Persistent organic pollutants such as organochlorine pesticides (OCPs) have been implicated in obesity and metabolic dysfunction. As they bioaccumulate in adipose tissue, OCPs may act as obesogens, but in vivo evidence for aldrin, endosulfan and lindane is limited. This study investigated whether subacute exposure to aldrin, endosulfan and lindane elicits obesogenic effects in male rats by examining weight gain, serum biochemistry and metabolic and inflammatory gene expression in white adipose tissue (WAT) and brown adipose tissue (BAT). Thirty-two adult male Sprague-Dawley rats were randomly assigned to receive corn oil (control) or oral aldrin, endosulfan or lindane (1 mg/kg every other day for 28 days). Body weight was recorded weekly. Serum liver enzymes and lipid profile were determined. In WAT and BAT, we quantified mRNA expression of thermogenic and adipogenic markers (Pparg, Ucp1, Ucp3, Fndc5), and the pro- and anti-inflammatory cytokines (Il-1b, Tnf-α, Il-10, Il-4). Lindane caused significant weight gain from the first week (p < 0.0001), whereas aldrin and endosulfan increased body weight only at week four (p < 0.05). Endosulfan-treated rats had reduced total and high-density lipoprotein cholesterol (p < 0.05) without changes in low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, or triglycerides. In WAT, Pparg, Ucp1, and Fndc5 transcripts were unchanged, while Ucp3 tended to decrease in the endosulfan group (p = 0.056). In BAT, endosulfan increased Ucp1 and decreased Fndc5 levels (p < 0.05), with no changes in Pparg or Ucp3. Endosulfan suppressed Il-1b, Tnf-α, and Il-10 (p < 0.05) transcripts in both WAT and BAT, and all pesticides reduced Il-4 expression in BAT (p < 0.05). Overall, short-term exposure to aldrin, endosulfan or lindane interfered with metabolic and inflammatory pathways in a compound-specific manner, with lindane causing early weight gain and endosulfan eliciting complex effects on lipid metabolism and adipose gene expression. We suggest that even short-term exposure to OCPs may affect metabolic regulation in male rats, with each chemical exerting distinct effects.